
Copyright^ 2l 

COPicRIGHX DEPOSIT 




GENERAL AND SPECIAL 

PATHOLOGY 

IN 

ABSTRACT 

(Illustrated) 

BY 

V B. WALLGREN, B. S., M. D. 

Assistant Professor of Biology, University 

of Pittsburgh; Pathologist to the 

St. Margaret's and Presbyterian 

Hospitals. Author Histology 

and Bacteriology. 



Second Edition 



Published by 

The Medical Abstract Publishing Company 

Jenkins Arcade Bldg. 

Pittsburgh, Pa. 



PREFACE TO FIRST EDITION 

IN preparing this Abstract on Pathol- 
ogy, the work of Stengel has been 
freely consulted, together with that of 
Adami, the Manual of Stenhouse and 
Pedersen, and others. 

It is not intended to take the place of 
a text book, but it is hoped that it will 
be of some use to the student and busy 
practitioner. 

A. B. Waugren. 

PREFACE TO SECOND EDITION 

The wonderful popularity of Pathology 
in Abstract has made it necessary to bring 
out a new edition which contains all upon 
the subject of Pathology that is found in 
the larger works. 

The author is actively engaged in Path- 
ological work in two hospitals, which is 
a guarantee that all of the advances that 
have been made are included in this book. 

The illustrations are taken principally 
from Stengel's Pathology. 

Publisher. 



MAY -6 1918 

©CIA495814 v " 



Copyrighted by 

The Medical Abstract Publishing Co, 

Pittsburgh, Pa. 



/ 



-\ ^ l8 PATHOLOGY.** ^* 

PATHOLOGY is the science of disease. 
It includes 

1. ETIOLOGY. Study of the causes of 
disease. 

2. MORBID OR PATHOLOGIC ANATO- 
MY. Study of structural changes. 

a. Gross Pathology. Naked eye ap- 
pearance of organ or tissue. 

a. Histological Pathology. Miscroscopi- 
cal appearance. 

3. MORBID OR PATHOLOGIC PHYSI- 
LOGY. Effects due to disturbance of 
function. 

Pathologic Chemistry— morbid chemical 

process and products during disturbed 

function. 
The expressions of abnormal functional 

activity are the Symptoms of 

Disease. 
DISEASE, is consequent upon an ab- 
normality in structure or function or 
both. 

Diathetic (constitutional predisposition) 
or hereditary (characteristics or tend- 
encies transmitted from parent to off- 
spring) conditions may f-equently lead 
to abnormalities or malformations. 

The ovum can transmit directly either 
disease or malformations such as 
syphilis, haemophilia, diabetes in- 
sipidus and color blindness, supernum- 
erary digits, webed-fingers and toes, or 
an individual can inherit through the 
same channel a predisposition for dis- 
ease such as gout or tuberculosis. 

The ovum during its growth has also a 
relation to future disease, in that por- 
tions "cell rests" may remain unde- 
veloped till some later period when it 
may begin to grow abnormally as a 
tumor. 

The ovum during its development is also 
subject to accidents which result in 

MALFORMATIONS— TERATOLOGY (A 

monster) 

Anamoly, a slight deviation from the 
normal structure but not so great as 



PATHOLOGY. 

to interfere with proper function. 
Monstrosity — when malformation is so 
great as to interfere with function of 
part or individual. 
. MALFORMATION DUE TO EXCESS. 

1. In size. 

a. General increase in size of individ- 
ual, as in a giant. 

b. Overgrowth of tongue. larynx, 
ringers or toes. 

2. In number. This is brought about by 
a varying degree of flsson of embryo. 
Division of ovum gives two complete 
individuals, more or less separate. 
If it occurs later in embryo there may 
be only reduplication of limbs. The 
growth may be equal or so unequal 
that one seems but an appendage of 
the other. 

a. Complete twin-monsters. 
Xiphopagus — union by xiphoid and 

umbilicus. 
Sternopagi — union from umbilicus 

upward. Double liver, lungs and 

heart. 
Prosopothoracopagi, (face). 
Syncephali (head). 
United by thorax and head. Single 

oesaphagus, stomach, duodenum 

and heart. Double lungs and 

urinary and sexual organs. 
Craniopagus — union by cranium. 

Brain may be single or double. 
Ischiopagus — union by pelvis. 
Pygopagi — union by buttock. 

b. Double parts. 

Diprosopus — double face; incapable 
of life. 

Dipyguo — single head and two 
bodies. Seldom seen in man. 

Parasitic form — one so poorly de- 
veloped it seems but a parasite 
on its fellow. 

Supernumerary arms and legs, 
fingers and toes. 

I. MALFORMATION DUE TO DEFECT. 

1. In cize. 
a. Dwarf — is defectively small but 
well proportioned, though the head 



MALFORMATIONS. 5 

is usually large, both body and legs 
are deformed. 

b. Micromelus — limb development is 
defective. 

c. Microbrachus — arm development is 
defective. 

d. Micropus — leg development is de- 
fective. 

e. Microcephalus — small head with de- 
fective brain development. 

2. In formation of parts. 

a. Homogenous Twins. Where one 
embryo is developed at the expense 
of the other. This may be caused 
by one having a stronger heart or 
a more rapidly growing allantois. 
Various conditions of the weaker 
gives rise to the terms, — 

a. Foetus papyraceus, (parchment 
like) shriveled up. 

b. Acardiacus — heart not developed. 

c. Omphalosites — receiving its nour- 
ishment through the allantois 
being attached to umbilical cord 
of the other. 

d. Acephalus and Acormus — hav- 
ing evidences of trunk and limbs 
but without head, heart or lungs. 

e. Amorphus — shapeless mass cov- 
ered with skin. 

3. Defective closure of Neural Canal. 

a. Anencephalus, Cranioschisis or 
Acrania, — brain and bones of crani- 
um are undeveloped, skull is open 
and eyes prominent — condition is 
called "toads head." 

b. "Encephalocele, hernia cerebri, — 
skull small, brain displaced to out- 
side. When ventricles are dropsical 
it is called — 

c. Hydrencephalocele. 

d. Cyclopia or Monophthalmia, — one 
eye with no retina in forehead, 
cerebrum has one ventricle. 

e. Agnathia, — no mandible. Often as- 
sociated with cyclopia. 

f. Spina bifida (cleft spine), — due to 
nonclosure of neural canal or rup- 
ture when closed. 



; pathology;. 

It is more often found in the lumbar 
region than cervical, 
li Rhaehischisis. — Central canal 

of cord, when present, open to ex- 
terior, inner surface of expanded 
membranes are continuous with 
unclosed edges of skin. 

2. Syringocele, — cord when pres- 
ent is dropsical and in this way 
forces cord through vertebral 
arches. 

3. Meningocele, — when arachnoid 
or subarachnoid is dropsical and 
spinal meninges alone appear. 

4. Myelomeningocele, — when both 
cord and meninges protrude. 

4. Defective Ventral closure. 

a. Aprosopus, schistoprospus, — non 
meeting of cranial and brachial 
arches, openings in mid-face, hare- 
lip, cleft palate, hydrocele of neck, 
cervical nstules, etc. are varities 
of this defect. 

b. Extroversio Vesicae, — fissure of 
bladder from failure of the allantois 
to close. Suprapubic abdominal 
wall is filled by posterior wall of 
bladder, Ureters open on its sur- 
face. Faulty obliteration of allan- 
toial communication with gut or 
genital organs may produce im- 
perforate anus and intestine may 
communicate directly with bladder, 
vagina or urethra. Other associated 
defects may be non closure of pubic 
bones, absence of urethra and 
clitoris and vagina of female, while 
in male the penis is not perfectly 
developed. 

C. Epispadias, — is where urethra is 
represented by a groove on the up- 
per surface of penis. 

d. Hypospadias, — is where urethral 
opening is on under surface of 
penis. 

5. Defective Extremities, — from acci- 
dent as adhesion of amnion, etc. 
Amelus— all limbs absent. 
Peramelus — defect in limbs. 
Phocomelus — hands and feet are at- 
tached directly to shoulders and 
hips. 



ETIOLOGY. 7 

Abrachius — without upper limbs. 
Perobrachius — portion of hand or 

arms defective. 
Apus — without lower limb. 
Peropus — portion of foot or leg are 

defective. 
Monobrachus — single arm. 
Monopus — single leg. 
Sirenomelia, symmelus or sympus — 
lower limbs are fused. 

Sympus monopis — limbs fused, 

only one foot. 
Sympus dipus — two feet fused. 
Sympus apus — limbs fused but 
without feet. 

IN. LATERAL TRANSPOSITION OF 
VISCERA. 

Various organs are found on side op- 
posite to normal situation. 

ETIOLOGY OF DISEASE. 

I. PREDISPOSING CAUSES.— System or 
parts is prepared for disease by render- 
ing it weaker or less resistant. A nor- 
mal organism is able to cope with the 
determining causes in disease but the 
resistance varies according to the in- 
dividual, race or varying climatic con- 
ditions. When a certain point of in- 
tensity in heat or cold or other causes 
of disease is reached the normal or- 
ganism is hindered or checked in its 
resistance and disease or injury re- 
sults. 

Resistance may be so great that certain 
diseases are not contracted, this is 
called immunity in contradistinction to 

Predisposition which is a weakness of re- 
sistance and may be divided into 

1. Hereditary. 

a. Abnormal weakness transmitted by 
parent to offspring. 

a. Direct from parent to offspring. 

b. Remote, where trait is latent. 

b. Congenital weakness not direct- 
ly heriditary but is more or less ac- 
cidental. 

2. Acquired — from previous disease, 
vices, etc. 

II. DETERMINING CAUSES— the im- 
mediate or specific cause. 



PATHOLOGY. 

1- TRAUMATISM — from whatever cause; 

effect depends upon the form 
the severity of injury. 

a. Pressure, — by disturbance of circu- 
lation or injury to cellular elements, 
may result in atrophy or a more 
destructive change — a necrosis or 
gangrene. 

b. Wounds, — may be so slight as only 
to cause inflammation and subse- 
quent regeneration, or so gross as 
to cause direct injury to tissue con- 
tinuity in a lesser or greater extent. 

2. PHYSICAL CONDITIONS, 
a. Heat in excess. 

1. Local excess, — depending upon 
degree, and varying accordingly, 
from relaxation of blood vessel 
walls, necrotic change in cellular 
elements and exudation of serum 
with vesicular formation to dis- 
truction, perhaps with charring, 
of areas, large or small, with 
hyperemia or reactive inflamma- 
tion of surrounding parts. Burns 
involving one-third or more of the 
body surface often cause death 
which is generally produced by 
formations of poisonous products 
of tissue distruction or disturbed 
functions of skin or organs. 
Immediate death is often from 
shock. 

2. Exposure to general high temp- 
erature. 

A constant temperature somewhat 
higher than the usual temperature 
will cause body to compensate 
its increased heat by increase in 
rate of respirations and pulse. 

Constant high temperatures may 
cause death by tissue-coagulation, 
particularly of muscle structures 
of heart and respiration. 

Constant excessive heat frequently 
causes conditions known as heat- 
stroke, sunstroke, insolation and 
heat exhaustion, due to direct ef- 
fect of the heat, or products of 
disturbed metabolism. 

From these, hyperemia, edema or 
inflammation of meninges may 
occur. 



ETIOLOGY. 9 

b. Cold. — Extreme degrees of cold 
may cause conditions like those pro- 
duced by heat. 

There is first vascular constriction 
then local anemia, which preserves 
body heat by lessening heat radia- 
tion; this is followed by vascular 
paralysis and extreme hyperemia. 
Cellular exudation and necrosis may 
occur. These changes are seen in 
condition called chilblain. In pro- 
longed cold exposure the activity of 
various organs is reduced, sensibili- 
ty weakened and coma gradually 
supervenes. 

Retention of metabolic excre- 
ments may be a party to this con- 
dition. 

The term cold is often used in con- 
nection with a pharyngitis or 
coryza but it is merely a predispos- 
ing factor, by reducing the resist- 
ing powers of the organism or alter- 
ing body fluids, thus favoring the 
activity of bacteria specific to a 
disease. 

c. Atmospheric Changes. 

a. Increased Atmospheric Pressure 

— as experienced in the work of 
deep-sea divers or men working 
in cassions, under pressure of 
several atmospheres, will fre- 
quently, on return to normal at- 
mospheric conditions, suffer from 
bleeding of mucus membranes, de- 
pression, delerium and paralytic 
conditions (cassion disease); this 
is due to vacuolations in spinal 
cord, depending of course upon 
the severity. 

b. Decreased Atmospheric Pres- 
sure — as experienced by inhabi- 
tants of high allitudes or in 
aeronauts. This is accompanied by 
vascular excitement as hemorr- 
hages and vomiting; in less mark- 
ed cases there is nervous excite- 
ment. The condition is probably 
due to want of oxygen and to less 
extent, directly to decreased ex- 
terior pressure. 

d. Insufficiency of Respiratory Air — 

due to obstruction of air passages 



10 PATHOLOGY. 

by disease or foreign bodies. The 
want of O as in CO 2 poisoning is 
due to displacement of O in 
hemoglobin of blood. 

Moderate decrease of air causes 
asphyxia (labored breathing, 

cynosis, depression and stupor.) 

Complete lack of air produces death 
by suffocation. Blood is dark and 
hemorrhages occur. 

A continued want of O may direct- 
ly or indirectly cause degenerations 
of tissues. 

e. Electrical Influences. — Electrical 
discharges may produce various 
damages to tissues such as burns, 
etc., often causing shock. The 
muscles, blood vessels and blood 
itself may be damaged extensively. 
The whole nervous system may be 
disturbed or even undergo degener- 
ation. Inhibition of heart may 
cause death. X Rays can cause cel- 
lular degenerations and necrosis 
with secondary inflammation. 

3. INTOXICATIONS— POISONS, are 

substances which will disturb the 
structure or functional activity of a 
living organism. 
They may be classified as: 

I. Inorganic, CO, CO 2 Cyanogen, lead 
mercury, etc. 

II. Organic. 

1. Artificial — chloroform, ether, alcohol, 
benzine, coffee infusions, etc. 

2. Dietetic — purin poisoning. 

3. Bacterial. 

a. Infectious diseases. 

b. Ptomains. 

1. Decaying meat, canned goods, 
etc. 

2. Kopraemia. 

4. Poisonous secretions and excretions 
from insects, snakes and tapeworm, 
maleria, etc. 

5. Metabolic. 

a. Uraemia. 

b. Acidosis. 

c. Leucomains (substances formed by 
action of living tissues in course of 
metabolism. 

d. Internal secretions. 



INTOXICATIONS. 11 

1. Diabetes. 

2. Exopthalmic goitre. 

3. Addisons disease. 

4. Acromegaly. 

They may be divided into: — 

A Exogenous Poisons, which enter body 
through wounds of the skin or sur- 
faces of the lungs, alementary or genito- 
urinary tract. From their action they 
may be divided into: — 

1. Local Poisons. Corrosives, escharotics 
and caustics. The effect is directly 
more superficial, producing a more or 
less disturbance to . cells with which 
they come in contact, in part by ab- 
straction of water and in part by their 
coagulating power. 

These poisons include acids, such as 
sulphuric, nitric, carbolic and hydro- 
fluric; alkalies, such as caustic potash 
or soda and ammonium; gases, such as 
chlorine and bromine; minerals, such 
as silver nitrate, mercuric chloride, 
copper sulphate, etc., and certain or- 
ganic bodies, such as croton oil and 
cantharidin. 

2. General Poisons, — manifested by 
changes in various organs or tissues 
of body by circulating in the blood. 
These may be divided into: — 

a. Organic or Parenchymal Poisons. 
Phosphorus, arsenic, lead, mercury, 
ergot, etc. The organs generally 
suffering most are the organs of eli- 
mination such as the kidneys and the 
mucous membrane of the intestines, 
which may show various forms of 
epithelial cell degeneration. Other 
organs of body sometimes affected 
are the liver, spleen, heart and blood 
vessels. Blood may also be affected 
secondarily. Toxalbumius of plants 
or toxic products of bacteria includ- 
ing bacterial action on various foods 
(ptomains-putref active compounds) . 
Decaying meat and shell fish, canned 
foods, etc., and the venom of serp- 
ents and various insects are also 
classed under organic poisons though 
they may also act as blood or nerve 
poisons or as all combined. 

b. Blood Poisons. 

1. Those combining with the hemo- 



12 PATHOLOGY. 

globin only as carbon monoxide, 
cyanogen, hydrogen sulphide. 

2. Those which change red blood cell 
and the coloring matter e. g. potas- 
sium chlorate, nitroglycerin, ani- 
lin, nitro-benzol, coal-tar products, 
arsenuretted hydrogen and poison- 
ous plants (toad stools). 

3. Those affecting blood and tissue 
generally such as abrin (from 
jequirty bean) and recin (from cast- 
or bean) cause a change in organs 
and increase coagulability of blood, 
hence thrombosis. 

4. Those which change blood-plasma 
or corpuscle, increasing or decreas- 
ing coagulability, e. g. calcium salts, 
carbonic acid and fibrin ferment 
increase coagulability, while albu- 
mose decreases coagulability. 

c. Nerve Poisons — produce alterations 

in nervous system. Change is gen- 
erally in central neurons causing a 
change in size of cells and nucleus 
with various degenerations or disap- 
pearance of dendrites and alterations 
in chromophilic bodies, etc. 
Some of these poisons are morphine, 
atropine, alcohol, chloroform, ether, 
etc. 

The venom of some serpents or ani- 
mals may act through nervous sys- 
tem though they are generally blood 
poisons. 

Ptomains may also act through nerv- 
ous system. 
B. Endogenous Poisons, — arising from the 
cells of the body. On account of the 
individual being poisoned by himself, 
as it were, the term autointoxication is 
used of this group. Poisoning from the 
bowel contents in chronic constipation 
(kopraemia) is sometimes called auto- 
intoxication, but wrongly so for the 
reason just given. 
METABOLIC DISTURBANCES. 

1. Decreased food supply; Inanition; 
Starvation. — The want of food or a 
gastrointestinal disturbance may lead 
to insufficient nourishment, causing a 
loss of body weight by consuming 
heat producing and energy giving 
substances. 



METABOLISM. 13 

Fats suffer first, then the carbohy- 
drates. 

Nitrogenous elimination is reduced. 
The chorides in the urine are de- 
minished and calcium salts are in- 
creased with destruction of osseous 
tissue. The various functions suffer 
and death may occur from exhaustion 
or secondary affections (acidosis.) 

2. Increased Food Supply, Overfeeding, 

— depends upon individual conditions 
and amount of exercise. Excess of 
proteid food increases excretion of 
urea. 

Excess of carbohydrates and fats in- 
crease the deposit of reserve fat and 
glycogen which may be used later and 
is physiological but an inordinate 
storing up of fat is probably 
pathologic as is frequently seen in 
Obesity, caused by excessive ingestion 
of food in those having an active di- 
gestion and leading sedentary lives. 
It is undoubtedly due to an inherent 
abnormal metabolism. 

3. Excessive Tissue distruction, — is in- 
dependent of amount of food ingest- 
ed. It is observed in fever, chronic 
infectious diseases with or without 
fever, tumors (carcinoma), intoxica- 
tions and some cases of Graves dis- 
ease. The nature of the "disturbance 
is obscure though ordinarily it is 
due to poisonous substances in the 
blood. 

4. Acidosis. Acid Intoxication. — Various 
acid bodies chiefly of acetone group, 
consisting of B-oxybuteric acid, 
diacetic and acetone derivatives of 
proteid decomposition are formed as a 
result of katabolism and their ac- 
cumulation in the blood on account 
of over production, interference with 
elimination, or a combination of the 
two, bring on symptoms as rapid 
respiration ataxia, convulsions and 
coma. 

The acids above mentioned together 
with lactic, sarcolactic, sulphuric and 
phosphoric are generally neutralized 
by the fixed alkalies (sodium and 
potassium) and with ammonium and 
in part excreted as such, the urea 
of urin is decreased and ammonium 



14 PATHOLOGY. 

salts are increased. Some, as sar- 
colactic acid are decomposed in the 
body and therefore rarely found in 
the urine. 

5. Formation of Albumoses, — due to dis- 
turbed metabolism and is present in 
the blood and excreted in the urine 
from fevers, suppurations or in tis- 
sue distruction of acute yellow 
atrophy, phosphorus poisoning, etc., 
ulceration of gastro-intestinal tract 
and some new growths. 

There is always rapid tissue dis- 
truction and its presence retards the 
coagulation of blood and causes 
leucocytosis. 

6. Aloxin Bases and Uric Acid — deriv- 
ed from the nuclein of cellular nuclei. 
Xanthin bases are intermediary pro- 
ducts which become more or less 
oxidized to uric acid. Normally uric 
acid is in excess of bases. Uric acid 
may be oxidized with the formation of 
urea. 

Cellular distruction, especially of the 
. leucocytes is the source of these pro- 
ducts. 

Gout is in some way dependent upon 
or associated with aloxin bases and 
uric acid. 

7. Glycosuria, is the occurance of grape 
sugar in the urine. It may be trans- 
ient or trivial in amount or it may 
manifest itself definitely as Diabetes. 
It is caused by the inability of the 
body to consume the carbohydrates 
and is due probably to a failure of 
certain preparatory stages in the de- 
composition of sugar molecule, hence 
cannot be oxidized by the tissues. 

4. VEGETABLE AND ANIMAL PARA- 
SITES, on entrance into the body are 
considered as specific cause of all in- 
fectious diseases. (See diseases due to 
bacterial and animal parasites). 
a. Bacteria (vegetable parasites). 
The term infectious is applied to all 
bacterial disease, but when the dis- 
eases are readily communicated 
from person to person the term con- 
tagious disease is used. Immediate 
contact is not always necessary. 
The term non-contagious is used 
when the transference is not ob- 



PYREXIA. 15 

served. It is a matter of degree 
only, as in some cases transference 
occurs through air, in others con- 
tact is necessary, in still others 
secretions or excretions of the dis- 
eased must be conveyed to the 
healthy. 

Endemic diseases are restricted to 
a locality. 

Miasmetic diseases are the same as 
endemic but are dependent upon the 
conditions of atmosphere, soil, etc.. 
for their continuance. 

Epidemic diseases affect a large 
number of people in a community. 
Pandemic diseases spread over large 
areas as country or continent. 
Bacteria may enter body by swal- 
lowing or inhalation; through abras- 
ions in mucous membrances or skir- 
and in utero from material to foetal 
blood. The nature and habitat of 
the bacterium together with sur- 
rounding conditions will regulate 
the mode of entrance in individual 
diseases. 
b. Animal Parasites, entering the 
body by invasion cause disease of 
various kinds. Some present a 
clinical picture of infectious diseases 
while other bear little resemblance. 

PYREXIA OR FEVER. 

A. fever is a rise in the temperature of 
the body above normal (98.6°F) due to 
increased metabolism especially in the 
muscles. In health the heat-produc- 
tion and heat-dissipation are balanced 
by the nervous system. In fever the 
production and dissipation are increas- 
ed though the latter is insufficient. The 
period of rigor or chill in fever, which 
is due to reflex spasm of the superficial 
arteries, though the internal tempera- 
ture is above normal, the metabolism 
is somewhat increased as proven by 
the increase in CO 2 excreted. During 
the fastigium acne or hot-stage, skin 
is hot, usually dry and glandular se- 
cretions are scanty. There is a great 
increase in the consumption of O and 
excretion of CO 2 but particularly of 
urea and extractives showing much 



16 PATHOLOGY. 

nitrogeneous waste. 
There may be a gradual decline of fever 
(lysis) or an abrupt termination 
(crisis), which is often associated with 
sweating, but with restoration of glan- 
dular function. 

Etiology. Commonly due to poisonous 
material entering blood in form of bac- 
teria or their toxines, or products of 
bacterial growth, which is probably of 
an albuminous nature. Other albumi- 
nous bodies resulting from normal or 
abnormal metabolism, such as albu- 
moses, peptone, tissue fibrinogen, etc., 
or ferments, as pepsin, fibrin-ferment, 
diastase, etc., may also produce fever. 
All these factors acting upon the nerv- 
ous system will produce fever, as will 
also excessive heat as seen in sun- 
stroke. Rarely is fever produced by in- 
juries or a disease of central nervous 
system as in tumors, degenerations, 
sclerosis, etc. 

Pathological Physiology. Loss of appe- 
tite, thirst, emaciation, more or less" 
disturbance of various organs. There 
is a tendency to inspissation of the 
blood. The corpuscles are relatively 
augmented and the specific gravity in- 
creased. The alkalinity of the blood is 
more or less reduced. 

Pathological Anatomy. There is a fall 
in blood pressure. Pulse and respira- 
tions are increased, due to influence 
of overheated toxic blood on heart 
muscle and the centers in medulla. 
Special lesions, depending upon the 
character of the disease, as cloudy 
swelling usually seen in liver, kidney 
and muscles, particularly the heart 
muscle, due to toxic blood. The con- 
dition may pass on to fatty degenera- 
tion or coagulation necrosis. 



DISTURBANCES OF THE CIRCULA- 
TION OF THE BLOOD. 

I. GENERAL DISTURBANCES. 
1. Weak Heart, due to 

a. Weakened heart muscle, from over- 
strain, fevers or other disease, ac- 
tion of poisons and insufficient nour- 
ishment, as in the anemias or nar- 



THE BLOOD. 17 

rowing of the coronary artery. 

b. Soft and cloudy, fatty or sclerotic 
heart muscle. 

c. Functional disturbance of intracar- 
diac ganglia. 

d. Diseased valves or orifices of heart. 
Results. Blood will accumulate in the 

venous system. The situation of the 
engorgement depends upon the part 
of heart weakened. 

If the left ventricle is weakened the 
blood backs to the left auricle and 
lungs. Congestion goes no further, 
but when right heart fails the right 
auricle and systemic veins are re- 
pleted. 

If right heart is first affected there 
is from the first a general venous 
congestion. Arterial pressure falls 
and blood current is slowed and 
venous pressure is increased. 
. Overaction of Heart, due tempor- 
arily to activeness of circulation and 
elevation of blood pressure. More 
lasting overaction is caused by over- 
work, excessive feeding or nervous 
stimulation, resulting in hypertro- 
phy of left ventricle, followed by 
whole heart with consequent over- 
active circulation. 

. Arterial Disorders. 

a. Organic disturbance. 

1. Sclerosed arteries impede ar- 
terial circulation. 

The heart compensates by hy- 
pertrophy. 

When the heart fails venous 
congestion and dropsy ensue. 

2. Localized conditions in aorta, 
such as narrowing, pressure by 
large glands or tumors, aneu- 
rysms, blood clots may inter- 
fere with the flow of blood, thus 
causing stagnation of the blood 
in the heart, lungs and veins. 

b. Vasomotor disturbances, due to dis- 
ease of nerve centers or toxic sub- 
stances which act locally on the 
vessels or upon the vasomotor cen- 
ter, causing constriction of the ar- 
terioles, with elevation of the blood 
pressure, slowing of the heart and 
venous congestion follows. 



18 PATHOLOGY. 

Contrary to this the arterioles may 
distend from vasomotor paralysis, 
with fall of blood pressure and hy- 
postatic congestion may follow. 

4. Blood Changes. A small decrease in 
the quantity of the blood is taken care 
of by the absorption of water from 
the tissues. A sudden large decrease 
in the quantity of blood may be fatal 
by syncope. A change in the char- 
acter of the blood by the accumula- 
tion of carbonic acid, and the product 
of tissue change may impede the cir- 
culation of blood by the toxic action 
on the terminal nerve filaments in the 
vessel walls or directly upon the 
walls, causing vasomotor contraction. 

II. HYPEREMIA— CONGESTION. Is an 

increase in the quantity of blood in a 
tissue or organ of the body. It is divided 
into — 

1. Active, Acute or Arterial Hyper- 
emia or Congestion. It is due to an 
increase of the blood flow to part. 
It occurs physiologically during the 
functional activity of the organs. 
Pathologically, it occurs from any 
condition which interferes with the 
nervous control of the calibre of the 
arteries, acting either — 

a. Through their local nerve plex- 
uses or the vasomotor center in 
the medulla. 

1. Neuroparalytic hyperemia. 
Vaso-constrictor fibers of the 
sympathetic nerves are cut off 
or compressed by tumors. 

2. Neurotoxic lryperemia. Vaso- 
dilator in the spinal nerves are 
stimulated as in neuritis. Toxic 
causes of fevers may act sim- 
ilarly through the vasomotor 
centers, causing superficial hy- 
peremia — 

b. by local affections of the vessel 
walls, from injury by — 

1. Heat. 

2. Traumatism. 

3. Inflammation. 

4. Drugs. 

5. Vascular fatigue, following 
temporary stoppage of the cir- 
culation, as frequently seen 



HYPEREMIA. 19 

on the removal of rubber 
bandage after a bloodless am- 
putation or in the abdominal 
vessels when the pressure of 
an ascites or large tumor is 
suddenly relieved. 
Arterial hyperemia is the initial 
phenomena of inflammation, but 
transudation only takes place 
when the capillary endothelium is 
damaged. 
. Passive or Venous Hyperemia is due 
to obstruction of the outflow of blood 
through the veins by — 
Failure of the left heart to provide 
arterial pressure. 

Failure of the right to empty the 
veins. 

Weak heart power, following attempts 
to overcome the obstruction in veins 
by thrombi, pressure by tumor, etc., 
or resistance of narrowed arteries 
(atheroma). 

These conditions bring on what is 
called — 

Hypostatic Congestion. The blood 

gravitates to dependent parts. It 
occurs frequently in low fevers. In 
combination with the continuous 
pressure on the skin of these parts 
congestion may result in necrosis 
with production of bed sores. In- 
ternally hypostatic congestion af- 
fects the lungs and pneumonia may 
follow. The congested areas are 
dark red (cyanosis). The capillary 
endothelium is ill nourished and al- 
lows the plasma of the blood to 
transude and the part becomes 
edematous and dropsical. In severe 
cases the red blood cell escapes by 
diapedesis. Passive hemorrhage 
may follow when congestion is very 
marked. 

Fatty degeneration from imperfect 
nutrition may occur later. 

If the hyperemia is moderate and 
long continued, overgrowth of con- 
nective tissue with pigmentation 
from broken down blood corpuscles 
(brown induration) generally fol- 
lows. 

When there is complete stoppage of 



20 PATHOLOGY. 

circulation in a localized area it is 

known as — 
Stasis, and if not relieved necrosis 
and gangrene will follow. 

III. ISCHEMIA OR LOCAL ANEMIA is 

the opposite to congestion, i. e., a tissue 
or organ contains less than its proper 
quantity of blood. 

1. Direct Ischemia is caused by — 

a. Pressure. 

b. General or local disease. 
Pressure may be due to bandages 

upon an organ or an area of body 
or upon the vessels within the tissue 
itself, as in amyloid disease or 
tumors. The circulation may be im- 
peded by sclerosis of vessels or 
emboli or thrombi within the ves- 
sel. Nervous influences acting 
through the vasomotor system, as in 
some gouty conditions and Ray- 
naud's disease, may produce a local 
anemia. 

2. Collateral Ischemia is due to the 
withdrawal of blood into hyperemic 
areas in other parts of the body, 
e. g., anemia of brain consequent to 
abdominal hyperemia. 

Ischemic areas are pale and cold, with 
atrophy and loss of function in pro- 
portion to the amount and perma- 
nence of the condition. 

IV. HEMORRHAGE is the escape of the 

constituents of the blood from its nat- 
ural channels. According to the vessels 
from which the escape takes place it is 
termed — 

1. Arterial. 

2. Venous. 

3. Capillary. 

4. Parenchymatous when it escapes from 
all of the vessels. 

From the mode of escape hemorrhage may 
be divided into — 

1. Hemorrhage per Diapedesim. Ooz- 
ing through capillary and smaller 
vein walls without any apparent 
rupture. The red cells and certain 
elements of the plasma escape. 

It is caused by the increased blood 
pressure, either active or passive, 
or the normal blood pressure with 
the increased permeability of the 



HEMORRHAGE. 21 

vessel walls due to degeneration of 
same by the action of poisons, in- 
fectious diseases, moderate injury of 
vessel, or temporary obstruction to 
the blood flow into a certain area. 
Altered states of blood may per- 
haps play a part when the vessels 
and pressure are apparently nor- 
mal. 
2. Hemorrhage per Rhexin, due to a 
break in the continuity of an artery 
or vein. 
Causes. 

a. Traumatism. 

b. Diseases of blood vessels from 
poisoning, infectious fevers, etc., 
degenerations and miliary aneu- 
rysm involving the intima or 
media. The outer coat may be 
eroded by surrounding disease, 
e. g., phthisical cavities. 

c. Increase of blood pressure. 

1. Absolute. 

a. Emotional excitement. 

b. Hypertrophy of heart. 

c. Paroxysms of whooping 
cough, etc. 

d. Asphyxia. The blood press- 
ure is increased from vaso- 
motor contraction and violent 
muscular efforts. 

2. Relative. 

Reduction of external pressure, 
e. g., balloon ascension or vio- 
lent inspiratory efforts when 
air cannot enter lungs. 

d. Neuropathic Hemorrhage, seen 
in — 

1. Some nervous conditions. 

2. Apoplexy. 

3. Epilepsy. 

4. Spontaneous hemorrhage from 
nose, stomach or into the lungs. 
This is also included in — 

5. Vicarious hemorrhage from sup- 
pression of menses. 

6. Stigmatization. 

7. Hemidrosis — sweating of blood. 

e. Hemorrhagic Diathesis — Hemo- 
philia. 

An hereditary condition. Persons 
affected are known as "bleed- 



22 PATHOLOGY. 

ers." The hemorrhage appears 
spontaneously or after trivial 
injuries or operations. 

In part, it is probably due to ex- 
treme thinness of the vessel 
walls and altered blood states. 

The condition is sometimes devel- 
oped as a result of various in- 
fections and intoxications. 

Classification. 

1. On free surfaces — from locality. 

a. .Epistaxis — nose bleed. 

b. Hemoptysis — from lung. 

c. Hematemesis — from stomach. 

d. Enterorrhagia — from bowel. 

e. Hematuria — urinary organs. 

f. Metrorrhagia — from uterus between 
menses. 

g. Menorrhagia — from uterus at the 
menses. 

2. From tissues — from size and nature. 

a. Ecchymosis. Infiltration of blood 
beneath the surface of skin and 
mucous membrane. 

1. Petechia — when small and well 
defined. 

2. Suggillation or sufusion — when 
large and diffuse. 

b. Hemotoma — blood tumor. 

c. Hemothorax — in pluera. 

d. Hemopericardium — in pericardium. 

e. Hematocele — in tunica vaginalis. 

f. Hematometra — in uterus. 
Results of Hemorrhage. 

Effused blood in small amount is 
taken up by the lymphatics. Re- 
peated small extravassations may 
lead to secondary anemia. In large 
amounts the corpuscle gradually 
breaks down into pigment, which 
passes into the lymphatics or de- 
posited at the seat of hemorrhage. 
The rest of corpuscle (fluid portion) 
is generally absorbed or may re- 
main as a cyst. A focus of hemor- 
rhage may act as a foreign body 
and become organized. It may also 
become calcified. It may also un- 
dergo degenerative changes. 
Large hemorrhages cause acute 
anemia, or a very large hemorrhage 
may cause sudden death by cere- 
bral anemia. 



THROMBOSIS. 23 

V. THROMBOSIS is the clotting of the 
blood in the blood vessel or heart dur- 
ing life. 
Causes. 

1. Alterations In the blood by the in- 
crease of fibrin forming factors as 
seen in typhoid fever, sepsis, etc. The 
activity of some bacteria in thrombi 
formation is probably due to their 
hemolytic action and injurious effect 
on the endothelium. 

Mineral poisoning and autointoxica- 
tions probably also form thrombi by 
their hemolytic power. 

2. Alterations in blood current, due to 
slowing of current from any cause, as 
narrowing of the vessels, weakness of 
the heart or pressure, as seen in 
various fevers and wasting diseases. 
The current may be slowed from dila- 
tations of the vessels, as seen in 
aneurysm or varicose veins; this in 
time causes degenerative changes of 
vessel walls, which is in addition gen- 
erally necessary. 

3. Changes in vessel wall, due to — 

a. Traumatism. 

b. Atheroma. 

c. Inflammations. 

d. Degenerations. 

e. Aneurysms. 

Pathologic Anatomy. 

1. White thrombi are formed from pure 
fibrin containing some leucocytes and 
conglutinated plaques. They are gen- 
erally formed slowly from actively 
flowing blood. 

2. Red thrombi are formed from fibrin 
and contain a large proportion of red 
corpuscles and indicate an almost 
complete or a temporary stasis of 
blood with a rapid production of 
fibrin ferment. 

3. Mixed or Stratified thrombi are made 
up from alternating red and white 
formations of thrombi due to the al- 
ternating slow and more rapid circu- 
lation of the blood. 

4. Hyaline thrombi is probably a com- 
pact form of the white. 

Effect. 

1. The blood flow may be compensated 
by collateral circulation. 



24 PATHOLOGY. 

2. Venous obstruction may cause 
venous congestion and dropsy. 

3. Arterial obstruction may cause 
eschemia, and degenerations and ne- 
crosis if blood' flow is not established 
by collateral circulation. 

4. Obstruction to small arteries may 
cause hemorrhagic infarction. 

5. Embolism, which, if infected, may 
produce general pyemia. 

Fate or Changes of Thrombi. 

1. Organization. The thrombus acting 
as an irritant to the tissues sets 
up an inflammation with the for- 
mation of connective tissue, which 
by its contraction forms new chan- 
nels, through which circulation is 
restored, or it may transform the 
vessel into a fibrous cord. 

2. Degenerations. The thrombi may 
be emulsified by liquefaction ne- 
crosis or fatty degeneration and 
pass into the blood stream as an 
embolism. Calcification of a throm- 
bus is frequent. 

3. Septic thrombi. A thrombus in 
blocking vessels of suppurating or 
necrosed tissue when infected by 
micro-organisms and undergoing 
softening may give rise to, general 
pyemia or an infectious embolism. 

VI. EMBOLISM. Foreign bodies of vari- 
ous kinds carried in the blood stream 
and deposited in the smaller arteries 
or capillaries so as to produce obstruc- 
tion are known as emboli. 
Source. 

1. Thrombi, in portion or whole from 
heart, large veins of the extremities 
or pelvis and atheromatous patches 
in the aorta. 

2. Fat, from bone marrow in fractures. 

3. Parasites. 

4. Masses of bacteria. 

5. Portions of tumor. 

6. Portions of calcareous heart valves. 

7. Portions of liver in accidental rup- 
ture of the organ. 

8. Placental cells. 

9. Disorganization of blood, as in the 
pigment particles in malaria. 

10. Small hyaline masses from burns and 
certain poisoning. 



EMBOLISM. 25 

11. Air. from rounds of large veins in 

neck, etc. 
Seats. Depend upon its source. 

1. An embolus derived from the left 
heart or from the -aorta passes to the 
general arterial circulation and finds 
lodgment in — 

a. Spleen. 

b. Kidney, 
c Brain. 

d. Other organs — peripheral vessels. 

2. An embolus derived from the general 
venous circulation is carried to the 
lungs, occluding the pulmonary circu- 
lation 

It may also reach the general arterial 
circulation when foramen ovale or 
ventricular septum is perforated or 
by being broken up into emboli so 
small as to permit passage through 
pulmonary capillaries. 

3. An embolus derived from the portal 
circulation may lodge in liver or pass 
through the liver into the heart and 
lungs. 

4. An embolus will sometimes be car- 
ried in the veins in a different direc- 
tion opposite to the blood flow. This 
is called — 

Retrograde embolism. It is seen in 
some pulmonary diseases causing in- 
creased intrathoracic pressure such 
as whooping cough, emphysema, etc. 
Results of an embolism depends upon 

its size and nature. 
1. From size — (purely mechanical). 
A large embolus occluding the main 
branches of the pulmonary or cere- 
bral artery or one of the coronary 
arteries may cause sudden death. 
If the vessel is not wholly occluded 
secondary thrombosis may complete 
the occlusion and death may be slow. 

The occlusion of less important ves- 
sels merely causes local anemia. 

An embolus caught at the bifucation 
of a vessel may break up into small 
pieces and produce multiple em- 
bolism of the branches. 

The obstructed artery contracts on 
the proximal side of the embolus 
and dilates on the distal side as do 
also the anastomosing branches of 







26 PATHOLOGY. 

neighboring vessels and circulation 
is quickly readjusted without serious 
or lasting damage to the tissues. 
The important mechanical result of 
small emboli is the pathological con- 
dition called — 

Infarction. 

An Infarct is the necrosed condition 
produced in the region of distribu- 
tion of an end artery by its ob- 
struction by an embolus. 

They occur in the periphery of an 
organ especially in the kidney, 
spleen, lungs, retina, base of brain 
and parts of heart. 

They are harder than the surrounding 
tissue and wedge-shaped with base 
towards the periphery of the organ. 
They are divided into — 

a. White or Anemic Infarcts are yel- 
low or grayish anemic wedge-shap- 
ed areas frequently surrounded by a 
zone of congestion or hemorrhage,.. 
The anemia is probably due to oc- 
clusion of the circulation and the 
area undergoing coagulation necro- 
sis. 

From the anemic period they may be 
changed directly, by the over- 
filling with blood and its extra- 
vasation, into an hemorrhagic in- 
farct. The persistence of the anem- 
ic form is due to the thrombosis of 
the venules receiving blood from 
the occluded endartery and anasto- 
motic capillaries or by the compres- 
sion of the capillaries by a rapid 
swelling of the parenchymatous cells 
of the organ. 

Some authorities contend that anemic 
infarcts may be formed by the 
absorption and the removal of col- 
oring matter of the blood from 
hemorrhagic infarcts. 

Infarcts of the spleen, kidney and 
brain are frequently anemic. 

b. Red or hemorrhagic Infarcts are 
dark red wedge-shaped areas of 
hemorrhage with coagulation. 

They are probably formed by the 
overfilling of the vessels from a 
back flow of blood from the veins 
or from free capillary anastomosis. 
The hyperemia produced leads to 



EDEMA. 27 

extravasation of the blood from the 
degenerative changes of the vessels. 

Lung infarcts are nearly always 
hemorrhagic. 

Results of Infarcts. 

In the red infarcts the extravasated 
blood breaks into pigment matter 
and the tissues undergo degenera- 
tions and is gradually absorbed. 
Reactive inflammation and organi- 
zation causes cicatrization with pig- 
mentation. The anemic infarcts 
undergo coagulation necrosis and 
caseation. 

A small amount of calcareous mat- 
ter is frequently deposited, es- 
pecially in the brain. In both the 
anemic and the hemorrhagic form 
the final result is scar formation, 
pigmented in the hemorrhagic form. 
Infarcts niay undergo liquefaction 
and cyst formation, especially in the 
brain. They may become infected 
with micro-organisms. 

2. From nature (which is septic). 

An embolus may contain micro-or- 
ganisms as is seen in cases of puru- 
lent softening of thrombi from, — 

a. Local suppuration or necrosis. 

b. Ulcerative endocarditis, etc. 
These may only cause an infarct 

which may become secondarily in- 
fected but micro-organisms gener- 
ally multiply and invade the tissues 
at once causing, — 

a. Suppuration. 

b. Gangrene. 

c. Metastatic Abscesses. 
VII. EDEMA AND DROPSY. 

The term Edema is applied to a condi- 
tion in which there is an accumulation 
of serum in the cellular tissue. 

It is brought about by an escape of serum 
through a more or less permeable mem- 
brane, the capillary walls, in conse- 
quence of direct filtration, osmosis or 
diffusion, and probably secretion of 
endothelial cells of capillaries and the 
hymphatic spaces. The quantity pres- 
ent in the tissue depends upon the 
amount escaping from blood vessels and 
the amount carried away by the lym- 
phatic system. 



28 PATHOLOGY. 

The term Dropsy is used indiscriminately. 
More strictly a general accumulation in 
the subcutaneous tissue and skin is call- 
ed Anasarca or hyposarca; local trans- 
udation is called oedema; dropsy of the 
peritoneal sac is called asites; in 
pleura — hydrothorax and in the pericar- 
dinum — hydropericardium, etc. 

Causes 

1. Increased blood pressure, always 
causes the escape of liquid from ves- 
sels (transudation) consequently 
more hymph. In active hyperemia the 
escaped liquid is carried off by the 
lymphatics and edema does not occur. 
In passive congestion, the escape of 
liquid is greater and lymphatic cir- 
culation is insufficient and edema or 
dropsy results. 

This is a process of direct filtration. 
The transudate consists of water, 
saline and a relatively small degree 
of albuminous constituents of plas- 
ma. 

2. Decreased tissue-elasticity and pres- 
sure, is probably only a contributing 
cause. It is a principal cause in 
edema ex vacuo where in the liquid 
of blood escapes to fill a place left 
vacant by disease or atrophy, as seen 
in subarachnoid spaces and other 
parts of the central nervous system. 

3. Alterations of the blood, probably 
act indirectly. Seen in the anemias, 
which will in itself cause increased 
permeability of the vessels, by ill 
nourishment or actually damaged 
endothelium by circulating toxic sub- 
stances. 

4. Alterations of the liquids of the tis- 
sues may cause increase in the diffus- 
ion of liquids. 

5. Increased permeability of the capil- 
lary-walls probably plays a part in 
every case of edema. 

Permeability is due to, — 

a. Diseased capillary walls from 

1. Degenerations, as in Brights dis- 
ease. 

2. Inflammations. 

3. Traumatism. 

4. Poisons. 

5. Bacterial toxins. 

b. Heredity. 



ATROPHY. 29 

Certain nervous conditions such as 

1. Neuritis. 

2. Neuralgia. 

3. Organic disease of the cord. 

4. Nervous irritations. 

6. Obstruction of the lymphatic cir- 
culation, infrequently produces 
edemia as the collateral circulation 
generally carries away the lymph. 
If a large trunk as thoracic duct or 
several smaller lymphatics are ob- 
structed edema may result. The 
former edema is known as chylous 
ascites and the latter is seen in 
elephantiasis. 

Pathologic Anatomy. Depends upon the 
situation. Liquid varies according to 
the cause. In transundates due to fil- 
tration, the liquid is watery with sp. gr. 
below 1016 and poor in blood corpuscles 
an albuminous matter. Where disease 
of the vessel walls, as inflammatory 
edema, plays a part, the liquid is more 
dense and contains more corpuscles and 
albumen. 

The transundate is found in the lymph 
spaces or in the interstices of the tis- 
sue. The part is swollen and boggy. 
The tissue pits on pressure and on sec- 
tion liquid exudes. This appearance is 
not so marked in the solid organs like 
the kidney or liver. 

Under microscope the tissue elements are 
seen to be pushed apart and the cells 
themselves may be diseased. 

Results. Function of part is impaired. 
Death may occur when epiglottis, lungs 
or brain is involved. Various cell de- 
generations of part and productive 
changes in the connective tissue may 
occur. 

RETROGRESSIVE PROCESSES. 

I. ATROPHY is a condition in which a 
tissue or organ decreases in size with- 
out definite disease of its parts. If a 
tissue or organ is under its normal size, 
due to defective development the con- 
dition is called hypoplasia. If an organ 
or part of body is entirely wanting, the 
condition is termed Aplasia. 

Causes. 

1. Want of functional demand. 



30 PATHOLOGY. 

a. Palsied limbs. 

b. Disturbance to trophic nervous sys- 
tem. 

c. Physiologic. 

1. Atrophy of thymus gland. 

2. Atrophy of the genital organs at 
the menopause. 

3. Involution of old age. 

2. Lack of use, as seen in muscle of a 
limb long confined in splints. 

3. Lack of nutrition from any cause 

either local or general such as, — 

a. Occlusion of vessels. 

b. Continuous pressure, as in athropy 
of the liver in women from tight 
lacing, or when an aneurysm esca- 
vates the vertebrae or the steady 
contraction of new connective tis- 
sue as in cirrhosis. 

c. Impoverished blood. 

Pathalogic Anatomy. 

1. Single or true atrophy. Individual 
cells are decreased in size without 
manifesting disease. 

2. Numerical. The cells are reduced in 
number and generally altered by some 
form of degeneration. 

In atrophy the parenchyma of an or- 
gan is the first to suffer. 

In the true form the cell may suffer no 
change except slight pigmentation due 
to the fact that the normal cell pig- 
ment does not suffer reduction. 

In other cases there may be a deposition 
of pigment from the blood and is 
known as brown atrophy as is often 
seen in heart muscle of old age or in 
cachectic disease. 

In other conditions cells may undergo 
various degenerations. 

Secondarily the connective tissue may 
suffer degeneration. 

Athrophic organs are often irregular, 
the consistancy may be more or less 
reduced or may be hard and tough 
due to the connective tissue hyper- 
plasia. The capsule is generally 
wrinkled. The color is often darker 
than normal. In the case of brown 
athrophy it may be decidedly changed. 
Pathologic Physiology. 

Function of organ is impaired, the 



DEGENERATION. 31 

amount of disturbance varyi ng accord- 
ing with variation in functions of the 
organ. 

II. DEGENERATIONS AND INFILTRA- 
TIONS. 

These two conditions may be said to go 
hand in hand and in individual cases it 
is often difficult to distinguish between 
two varieties. 

Degeneration is the retrograde change 
which takes place in a cell or tissue by 
which their integrity is altered in the 
direction of lowered vitality. The pro- 
toplasm of the cell may be converted 
into substances abnormal to it in kind 
and quantity. The cell may break down 
and be absorbed or its altered debris 
may remain in one form or another. 

Infiltration is the deposit, in the cell from 
the blood or other fluids of the body, of 
a foreign substance which may remain 
either within the cell as a fat or pig- 
ment, or it may be found around the 
cell as in the amyloid degeneration. In- 
filtration frequently interferes with cells 
function. 

1. Cloudy Swelling; Albuminous Infiltra- 
tion; Albuminous, Parenchymatous or 
Granular Degeneration is an edema of 
cellular protoplasm with granular 
change of the protied and production 
of opacity. 

Causes. 

a. Intoxications. 

1. Bacterial toxines. 

2. Organic substances. 

3. Inorganic substances. 

b. Hyperpyrexia. 

c. Inflammations. 

d. Nutritional disturbances. 
Pathologic Anatomy. 

The organs are sometimes greatly en- 
larged, doughy and on section may be 
found dull gray in color, a little moist, 
and protruding parenchyma. 
Microscopically the cell is finely opaque, 
due to refractile granules. 
The normal protoplasmic granules may 
have disappeared and vocuolations may 
also be observed. The nuclei may be 
obscured by granulations. 
The chromatin is diffusely stained, but 
in the late stages the cell stains very 
poorly if at all. 



32 PATHOLOGY. 

Pathologic Physiology. 

The coagulation is due to precipation or 
coagulation of a part or all of the cells 
protied. The function of organ is more 
or less interferred with. Recovery is 
frequent. If causes persist fatty de- 
generation generally follows. 
Seats. Glandular epithelia and muscle 
fibers. 

2. Hydropic Degeneration or Dropsical 
Infiltration is the presence of a fluid 
in the protoplasm of the cell. 
Causes,— probably a physical phenom- 
ena in the dropsies, also a part of 
cloudy swelling. Burns and other skin 
lesions. 

Inflammations. 

Pathologic Anatomy. 
Microscopically, the cells are swollen 
even to bursting and clear from sep- 
aration of their contents. The fluid 
may be between the cells, often com- 
pressing them noticably. 
Pathologic Physiology. The protoplasm 
sooner or later becomes cloudy and 
often undergoes fatty degeneration. 
Vacuolation is frequently observed. 
Seats. 
Inflamed tissues and cancer. 

3. Fatty Infiltration, is the deposition of 
fat in cells which normally contain none 
other deposition, in excess, of fat in 
cells, normally containing it. 

Causes. 

a. Physiologic. 

1. Puberty. 

2. Pregnancy. 

3. Menopause. 

b. Pathologic. 

1. Inherited tendency. 

2. Luxurious living with lack of ex- 
ercise. 

3. Exceptional digestive power and 
faulty combination. 

4. Alcohol. 

5. Cachexias, as the fatty liver some- 
times seen in phthisis and in the 
cells of carcinoma. 

6. Organic disease of the nervous sys- 
tem. 

7. Bone disease. 

8. Fracture, or bone operations. Fat 
is taken up by the circulation. 



DEGENERATION. 33 

9. Diseased or atrophied organs or tis- 
sues. The deposition may take place 
around a sclerosed kidney or in 
bones, also in muscles in pseudo- 
hypertropic paralysis. 

Pathologic Anatomy. 

The appearance varies with the tissue 
affected. The connective tissue is 
usually affected . Microscopically the 
infiltrated tissue looks like that of nor- 
mal adipose- tissue. In the connective 
tissue the deposit of fat may be local- 
ized or diffuse or in streaks along the 
planes of fascia or fibrous strands, un- 
der endothelial membranes, about 
lymph channels, between muscular 
fibrillae or under the skin. In the or- 
gans, such as the kidney, the fat is 
seen around the tubules; in the liver, 
in the trabeculae, also in the hepatic 
cells; in the heart between fiber 
bundles and under the serous mem- 
brane. 

In the parenchyma cells the fat is seen 
as distinct drops within the cell wall. 
Where there is much fat in the cell 
the cell protoplasm is crowded to the 
cell wall, and the nucleus is flattened, 
though normally distinct, and stains 
easily. 

Pathologic Physiology. 
Unless very extreme the functions of 
cells are not greatly embarrassed and 
complete recovery is the rule. It may, 
however, lead to secondary conditions, 
as mechanical embarrassment or de- 
generations, which may be serious ac- 
cording to the organ involved. 

Seats. 

Subcutaneous and subserous tissues, 
mesenteries and omentum, along fascia, 
between muscles, kidney, liver and 
heart. Lungs and central nervous or- 
gans rarely. 

4. Fatty Degeneration is a destructive 
chemical change of a cell protoplasm 
into fat. 
Causes. 

a. Cloudy swelling. 

b. Intoxications. 

1. Metallic, as mercury, arsenic, lead, 
etc. 

2. Compounds, carbonic oxid, chlor- 
ates, coal tar compounds, pyrogallic 



34 PATHOLOGY. 

acid, chloroform, etc. 
3. Toxines of bacteria. 

c. Anemias and cachexias. 

d. Extreme hemorrhage. 

e. Metabolic disease. 

f. Fever if high and prolonged. 

g. Fatty infiltration. 

h. Trophic disturbances. 

Pathologic Anatomy. 

Organs are generally increased in size 
(except in acute yellow atrophy of 
liver, etc.), consistency is generally de- 
creased, the sp. gr. reduced, color is 
generally pale yellow, though conges- 
tion or pigmentation will alter this. 

The degenerated areas may be uniform 
or isolated. On section, fat may drop 
from knife and cut surface. Microscop- 
ically, parenchyma cells are primarily 
affected; connective, tissue may at 
times be involved. Cells are usually 
enlarged. The granules of the proto- 
plasm disappears, to be replaced by 
fine dark granules, which stain black 
with osmic acid, and are dissolved by 
ether or alcohol, but not by acetic acid. 
The fat is generally seen as numerous 
droplets, though they may become one 
drop, as in fatty infiltration. The chro- 
matin of nuclei becomes diffuse and 
stains poorly, or it may disappear. 

The cell membrane sooner or later breaks 
down and fatty contents and detritus 
fill the space. Cholesterin, lecithin and 
fatty crystals are often seen. 

Pathologic Physiology. 
Fatty degeneration results from an in- 
filtration of fat derived from the blood 
and from fat deposits of the body, or 
from food, and deposited in diseased 
cells. Fatty degeneration tends to 
cause secondary changes in the cells 
protoplasm or the fatty degeneration 
itself will increase until the cell is de- 
stroyed. In mild cases where nuclei of 
cells are not destroyed recovery may 
take place. Severe grades go on to total 
necrobiosis. 

Seats. 

Occurs in nearly all tissues. Most fre- 

. quent are the epithelial structures, such 
as liver, kidneys, heart muscle, central 
nervous organs. 

"Interstitial and ..parenchymatous tissues 



DEGENERATION. 35 

may be involved. 
Exudates and transudates are liable to 
the change, and liquid may give the 
appearance of an emulsion. 
5. Albuminoid Degenerations. 

This condition represents a proteid 
metamorphosis. There are four varie- 
ties, and, though they have several fea- 
tures in common, especially in their 
chemical composition and microscopic 
appearance, they may be distinguished 
by their reactions and by their prefer- 
ence for special tissues and sites. 
a. Mucoid Degeneration is the conversion 
of cellular protoplasm into mucin. 
Causes. 

Mucin should not always be consid- 
ered pathological, as we find it physio- 
logically in glandular epithelum, um- 
bilical cord, chorionic villi and the 
vitreous humor, nor should the hy- 
persecretion of mucin, as a result of 
inflammation or irritation of all sorts, 
be mistaken for mucoid degeneration. 

1. Inflammation. 

2. Myxedema. 

3. Scleroderma. 

4. Tumors. 

The occurrence of mucin in sarco- 
mata, carcinomata, fibromata, lipo- 
mata or chondromata is accidental, 
though occasionally it may be a 
direct transformation, as is the case 
in myxomata. 
Pathologic Anatomy. 

On mucous membrane it appears as a 
coat of thick, tenacious mucus, with 
or without congection or other changes. 
Where it is pent up in the tissues it 
swells, dilates the chambers and flat- 
tens the epithelium, and later becomes 
a thin albuminous fluid and takes on 
the appearance of a cyst. In connective 
tissues it may not show the mucin 
characteristics, but the tissue is soft, 
elastic and tears easily. 
. It is insoluble in water, though it will 
take up water and swell. It is very 
soluble in alkaline solutions, but is pre- 
cipitated by alcohol, heat, many of the 
metals, acetic acid and "on saturation 
with most neutral salts. 
Mucin from cystic ovarian neoplasms is 
often . peculiar, . in that . it , will not pre- 



36 PATHOLOGY. 

cipitate with acetic acid, and is there- 
fore called pseudomucin. 

Microscopically. In mucous membranes 
the goblet cells are excessive in quan- 
tity. Death of cell occurs only in ex- 
treme cases. The cells are much swol- 
len, with distal end bulged out with 
mucin. The submucous tissue is usually 
inflammatory and pus cells containing 
mucin may be seen. In the connective 
tissue the mucin lies between the cells, 
the ground substance of which has dis- 
appeared. 

The cells themselves, though rarely 
changed to mucin, may be degenerated 
otherwise. In tumors the change may 
be in and between the cells or in the 
form of cysts. Mucin is fixed by the 
bichloride of mercury. It stains with 
most of the basic analin stains. Thio- 
nin and toluidin blue stain the nucleus 
blue and the mucin red. It is, how- 
ever, not entirely distinctive. 

Pathologic Physiology. 
Causes and modus operandi are not 
clear. Unless the disease is prolonged 
the tissue affected may recover. 

In connective tissue the deposit may often 
be removed by reabsorbtion. In neo- 
plasms it is probably an evidence of 
cell death. 

Seats. 

Epithelial tissues of the respiratory and 
gastro-intestinal tract, salivary glands 
and uterus, though any epithelial tissue 
may be involved. 

Skin, any connective tissue, ovarian 
cysts, carcinomata and any mesoblastic 
tumor. 

b. Colloid Degeneration is the abnormal 
appearance in the tissues of a colloid 
substance, like that found in the thyroid 
glands. 

Causes are obscure. 

It may arise from or be converted into 
mucoid material and borders on the 
hyaline substance. It occurs in 
goiter and thyroid neoplasms and 
other organs of the body. 

Pathologic Anatomy. 

The tissue affected is the connective 
tissue. The organs affected are en- 
larged, hard or soft. On section the 
areas involved appear as yellowish- 



DEGENERATION. 37 

brown, translucent bodies, sometimes in- 
visible, sometimes they may be in form 
of large cysts. 

A serous transudation may accompany 
the colloid degeneration and dissolve it, 
so that the cysts may be filled with a 
chocolate-colored fluid containing pus, 
blood, cholesterin, sodium chloride and 
calcium oxalate. 

Microscopically. The material is found in 
the cells, in the glandular acini and in 
the connective tissue. 

It is generally arranged in balls or 
whorls. The cells generally show de- 
generative changes and inflammation is 
often present. 

The material shrinks, but is not precipi- 
tated by acetic acid or alcohol. 

Stains with acid stains. It does not stain 
with I. & K. I. or methyl-violet. 

Pathologic Physiology is obscure. 
The substance is undoubtedly formed 
in loco. It is grave and usually asso- 
ciated with marked cellular disturb- 
ance. It may be changed into mucoid, 
hyaline or be replaced by an exuda- 
tion. 

Seats. 

Thyroid gland, kidney, prostate, pituit- 
ary body, parovarium and carcinomata. 

c. Amyloid Degeneration is the appear- 
ance in the tissues of an amyloid sub- 
stance. 

Causes. 

1. Suppuration and ulceration, as seen 
in tuberculosis of lungs and bones, 
syphilis, various gastro -intestinal ul- 
cerations and in actinomycosis. 

2. Mixed infections. 

3. Without suppuration (rare) in the 
cachexias, as in cancer, materia, 
leukemia, etc. It may sometimes be 
found without any apparent cause. 

Pathologic Anatomy. 

Organs are enlarged and specific 
gravity is increased. On section they 
are firm and smooth. The consistency 
may vary according to the degree of 
fibrosis, fatty degeneration, etc. It is 
generally inelastic. The color is pale, 
though this may be altered by con- 
gestion, pigmentation or fatty degen- 
eration. 



38 PATHOLOGY. 

The amyloid substance is translucent, 
glistening and waxy. 

Microscopically. It is found in the outer 
surface of the capillary walls, the in- 
tima and media of the larger blood 
vessels (the adventitia being rarely af- 
fected and the endothelia probably 
never), fixed connective tissue of the 
organs, elastic tissues and basement 
membranes of the glandular acini. The 
material appears as irregular clumps or 
streaks in the interstitial tissues, often 
compressing the cells and blood vessels. 
The cells are generally atrophied and 
degenerated otherwise. 

The material is insoluble in water, alcohol 
and weak alkalies. It swells, but is in- 
soluble in the tissue fluids. 

It stains a light pink or red with gentian 
violet or iodine green, a mahogany red 
with Lugol's solution of iodine. The 
red color is changed to blue by treat- 
ing with sulphuric acid or chloride of 
zinc. 

Pathologic Physiology. 

It is a combination of chrondratin sul- 
phuric acid with a proteid. 

As chrondratlnic acid is normally present 
in the tissues (bone, cartilage, elastic 
tissue) of the body it is probably not 
abnormal, but an abnormal combina- 
tion of normal substances. 

Local cellular conditions probably favor 
the deposition of the material by rea- 
son of their inability to properly dis- 
pose of the constituent substances 
brought by the blood. 

Hyaline degeneration may be a prelim- 
inary stage. 

The functional activity is interfered with 
by reason of pressure upon the paren- 
chyma and by vascular disturbances. 
It may occasion thrombosis by reason 
of its situation. 

Reabsorbtion has been known to take 
place, but not when extensive change 
exists. 

Seats. Glomeruli of kidney, liver, spleen, 
blood vessels, endocardium, intestinal 
mucosa, lymph glands, adrenalin bodies, 
dural tumors and in rare cases the vol- 
untary muscles and nervous system. 

d. Hyaline Degeneration is the appear- 




Fig*. 1. Cloudy swelling' and necrosis 

of the epithelial cells of the renal 
tubules, due to sublimate poisoning:. 
(Kargr and Schmor.) 




i .*<« 



r i 






Fig. 2. Colloid degeneration of the 
thyroid gland, showing- masses of col- 
loid matter in the gland acini. (Kargr 
and Schmor.) 




Fig. 3. Amyloid defeneration of the 
kidney, showing- amyloid substance in the 
walls of the blood vessels of the glome- 
rulus at b, and hyaline tube casts in 
the renal tubules at g. (Ziegler.) 




: - ^* v '1'*" -*- 






-.. vr-, .«*•*. 









Fig:. 4. Coagulation necrosis of the 
hepatic cells in a case of puerperal 
eclampsia. (Karg and Schmor.) 



DEGENERATION. 39 

ance in a tissue of a homogenous pro- 

teid substance of an obscure nature. 

Causes. 

It is allied to the other albuminoid de- 
generation and can pass into each of 
them. It is also related to coagula- 
tion necrosis. It occurs under the 
following pathological conditions — 

1. In muscles during infections and 
septic processes; also after trauma- 
tism. 

2. Intoxications, as by lead. 

3. In interstitial hemorrhages and 
hematoma. 

4. In struma. 

5. Cicatrices. 

6. In blood vessels of old age. 

7. In arteritis. 

8. In disease of endocardium and car- 
diac valves. 

9. In granulomata. 

10. In neoplasms. 

11. In lungs in pneumonia. 

12. Nephritis. 

13. Coagulation necrosis. 

14. Fibrinous exudation. 

Pathologic Anatomy. 

If extensive enough to be macroscopic 
the tissue or organ is enlarged, dense, 
pale and opaque. On the mucous or 
serous membrane small collections, 
pseudomembraneous or opaque plaques 
may be seen. 
Microscopically, it is found in three sit- 
uations — 

1. In the blood vessels, where it may 
be in or beneath the endothelium, 
surrounding the vessel, or between 
its coats or fibers. 

2. In the interstitial tissue. 

3. Within the cells. 

Unstained it has a glistening, waxy ap- 
pearance, but is less translucent than 
amyloid. It has an affinity for acid 
anilin stains. It may also take basic 
stains in a modified manner. 
A mixture of picric acid and acid 
fuchsin (Gieson's) will stain it red. 
Pathologic Physiology is obscure. It con- 
sists probably of a proteid modified in 
loco by a disturbed action of cells, or 
it may be brought by cellular carriers. 

It can be reconverted, absorbed and re- 
moved. It will not interfere greatly 



40 PATHOLOGY. 

with parenchymatous structure. 

It may be converted into other albu- 
minoid degenerations and may undergo 
caseation or calcareous infiltration. 

Seats. Cardiovascular system, muscles, 
mucous and serous membranes, liver, 
kidney, spleen, ovaries, adrenal bodies, 
nervous system and neoplasms. 

6. Glycogenic Infiltration is the presence 
of glycogen in cells which normally 
contain none or an excess in cells which 
normally contain it. 

Causes. 

Glycogen is normally present in the 

liver, muscles, leucocytes and blood 

serum. 
It occurs pathologically in the blood of 

diabetes and cachectic states. 
Pathologic Anatomy. It is generalby mi- 
croscopic. The substance is usually 
found within the cells. It is sometimes 
found in the intercellular substance and 
may be free in the blood or fluid of 
exudates. It is seen as round balls con- 
centrically striated. 
If fresh it is soluble in water, but loses 
its solubility after alcohol fixation. It 
stains brownish red with iodine, but 
sulphuric acid does not turn it blue. 
There is loss of color reaction when 
treated with ptyalin or amylopsin. 
Pathologic Physiology is obscure. In neo- 
plasms and suppurations it is probably 
deposited. 

Seats. Kidney, blood, purulent collec- 
tions and inflammatory areas, malig- 
nant growths of mesoblastic origin. 

7. Calcification is the abnormal deposition 
in the tissues of earthy salts, chiefly the 
phosphates and carbonates of lime and 
magnesia. 

Cause. 

1. Vascular disorders in diseased tissues. 

2. Local necrosis or fibrosis. 

3. Neoplasms. 

4. Degenerations, especially fatty and 
hyaline. 

5. Old age (due to increased lime re- 
absorbtion from the skeleton). 

6. Extensive disease of bones. 
Pathologic Anatomy. No early macro- 



DEGENERATION. 41 

scopic signs are present. However, in 
the gross it is gritty or of stone hard- 
ness and grates on the knife. On the 
addition of a dilute mineral acid 
earthy material will dissolve with for- 
mation of carbonic acid. 

Microscopically. It is opaque by trans- 
mitted and glistening by reflected light. 
The granules are fine and scattered 
through the intercellular substance. In- 
frequently the cells show an infiltration 
with more or less extensive degenera- 
tions. The granules may coalesce and 
assume a concentric arrangement 
(psamomma bodies). 

Calcarious plates are formed in the blood 
vessels and serous membranes. 

In blood vessels and neoplasms deposits 
may be great. The color is here white, 
grayish or yellow. A discoloration is 
due to pigments. 

It stains by carmine and hematoxylin, but 
not as a rule with analin dyes. 

Pathologic Physiology. 
It is considered by some to be due to 
an escape of carbonic acid from stag- 
nant lymph, with consequent precipita- 
tion of the earthy salts; by others to a 
combination of these salts with the 
albumins and fatty acids of the degen- 
erating tissues. 

It is probable that the salts are precipi- 
tated as insoluble combinations with 
proteids. The deposits are seldom if 
ever removed. They will cause degen- 
erations of adjacent tissues. 

Seats. 

1. Cardiovascular system (affecting 
chiefly the intima and media). 

2. Hyaline cartilage (except articular 
cartilage). 

3. In tissues subject to pathologic 
change. 

4. Ganglion cells of brain. 

5. Renal cells. 

6. Tumors. 

7. Cicatricial tissue. 

The foetuses of extrauterine pregnancy 
are sometimes calcified and are then 
known as lithopaedion. 

In some cases true ossification occurs 
where only calcification might be ex- 
pected. An accurate differentiation 



42 PATHOLOGY. 

from calcification can only be made 
where osteoblasts are detected after 
the material is decalcified. 
Uratic Infiltration. The deposit of urate 
of sodium in cartilages and fibrous tis- 
sue of joints, etc., occurs in gout. 
8. Pigmentation. According to origin and 
variety of pigments it may be divided 
into— 
a. Pigmentation from External Causes. 

1. Entering through air passages and 
termed pneumonokoniosis. 

a. Coal pigmentation called anthra- 
cosis. 

b. Iron pigmentation called side- 
rosis. 

c. Stone pigmentation called calci- 
cosis. 

d. Vegetable particles. 

e. Animal hairs and furs. 

This is commonly an occupation 
disease. Inhaled substances are 
probably caught by the cellular 
cilia of the bronchial tubes and 
coughed up or eliminated with the 
bronchial secretions. Some of the 
substance penetrates the bron- 
chial wall or is carried into the 
submucosa and deposited in this 
situation by the phagocytes, or it 
may be carried by the lymph to 
the peribronchial and mediastinal 
glands, fibrous tissue of lungs or 
the subpleural tissue. 

In rare cases the pigment enters 
the general circulation and is de- 
posited in the various organs of 
the body. 

2. Entering through the alimentary 
canal. Due to an excessive inges- 
tion of soluble metallic salts, such 
as silver, etc. If due to silver salts 
the condition is called argyra. 

b. Pigmentation derived from the hemo- 
globin called Hematogenous Pigmenta- 
tion. 
The pigments are — 

1. Siderous, which is chiefly hemo- 
siderin. 

2. Non-siderous, derivatives of hema- 
tin, hematoidin, hemofuscin, me- 
lanin, etc. 

Hematogenous Pigmentation is divided 
into — 



DEGENERATION. 43 

1. Those in which the hemolytic 
agents act in the blood; found in — 

a. Pernicious anemia. 

b. Leukemia. 

c. Malaria. 

d. Cachexias. 

e. Infectious and septic processes. 

f. Poisoning. 

The hemoglobin is set free in the 
blood. It is eliminated by the kid- 
ney and to a small extent by the 
intestines. It is converted into bile, 
a little passing into it unchanged. 
Some is reduced by the tissues to 
the siderous and non-siderous, and 
is then carried by the lymph and 
blood stream and is deposited by 
cellular carriers in various places 
in the body. The depositions are 
both inter and intracellular. 
Hemochromatosis is a condition in 
which a pigment containing iron is 
deposited in the epithelia of the liv- 
er and pancreas, and a pigment free 
from iron in the smooth muscles of 
the intestines, walls of the blood and 
lymph vessels and in the connective 
tissue. Associated with this pigmen- 
tation was cirrhosis of the organs. 
The diabete bronze of the French is 
a widespread form of this pigmen- 
tation, in which, in addition, other 
organs and skin are involved. It is 
accompanied by glycosuria, due to 
cirrhosis of the pancreas. 
Alcohol, cachexia and other toxe- 
mias are of etiologic importance. 
The deposits in the cells cause de- 
generations and death of same. 
The appearance of the organs vary ac- 
cording to the variety and stage. 

2. Those in which reductions occur in 
local tissues — 

Local pigmentation. 
Causes. 

a. Thrombosis. 

b. Interstitial hemorrhage and co- 
agulation. Pigmentations of in- 
duration result of venous stag- 
nation, and congestion are 
probably of the same origin. 

The pigment is diffused from the 
blood cell; some is carried away 
by the plasmatic circulation. 



44 PATHOLOGY. 

When areas become enclosed the 
pigments are formed within. The 
pigments change and are then 
carried away by the phagocytes 
to various parts of the body, es- 
pecially to the liver, blood modi- 
fying organs, intestines and 
glands; the deposits being known 
as pigment- metastasis. Micro- 
scopically the pigments are found 
as small needles, rhombic crystals 
or amorphous masses or small 
clumped balls. The color varies 
from pink to deep red; from yel- 
low green to brown or black. 

c. Pigmentation derived from the Bile. 
Hepatogenous Pigmentation. 

It is due to bilirubin and biliverdin. 
All jaundice is of hepatic origin. The 
pigments deposited are either in so- 
lution in the tissues, in precipitation 
or crystals. The liver, skin, mucous 
and serous membranes, endarterium. 
glandular and fatty tissue are very 
susceptible. 

The color is first yellow, then deepens 
to olive. 

d. Pigmentation derived from cellular ac- 
tivity within the organism. Metabolic 
Pigmentation. 

Pigments are probably formed by mi- 
gratory and pigment-building cells 
and deposited by means of the 
leucocytes and plasma cells. 

The hemoglobin has secondarily some- 
thing to do with its manufacture 
with the possible exception of some 
pigments of melanosarcoma. 

This pigmentation may be — 

1. Local, as seen in — 

a. Nevi. 

b. Moles. 

c. Pregnancy. 

d. Corpus luteum. 

e. Freckles. 

f. Scars. 

g. Certain skin disease. 
h. Melanosarcomata. 

2. General, as seen in — 

a. Addison's disease.. 

b. Severe anemias and cachexias. 

c. Tuberculosis of peritoneum, in- 
testines and retroperitoneal 

.;.. . . glands. 



NECROSIS. 45 

d. Abdominal neoplasms. 

e. Senility. 

Metabolic pigments are generally de- 
posited as granules, sometimes crys- 
tals, in and between the cells. 

9. NECROSIS is the local death of tissue. 
Necrobiosis is the death of individual 
cells. 

Causes. 

(1) Circulatory derangements. 

(a) Acute and chronic ischemia, 
produced by embolism thrombosis, 
arteriosclerosis, atheroma, extra- 
arterial blood pressure, cardiac 
spasms, as ergotism and Ray- 
naud's disease. 

(b) Venous stagnation. 

(c) Aneredas. 

(d) Cachexias. 

(e) Senility. 

(f) Diabetes. 

(2) Trophic derangements, due to 
trophic disturbances, as in bed sores 
and myletic cystitis. 

(3) Intoxications, due to animal, 
vegetable, bacterial and inorganic 
poisons. 

(4) Traumatism, due to pressure per 
se or the pressure of calculi, con- 
cretions, enteroliths and exostoses. 

(5) Inflammations. 
Varieties — 

a. Coagulation Necrosis. In this necrosis 
the proteid of the tissue suffers death 
from changes similar with coagulation. 

Pathologic Anatomy. 

Macroscopically. The tissue is of a 
glazed, opaque, waxy appearance, 
pale and firm. 

Later the tissue becomes grayish and 
is inclined to soften. 

Microscopically. There is a fixed exu- 
date in the tissues. Fibrin granules 
or fibrills are present. Fibrinoids, 
which do not react to stains like the 
fibrin, are also seen. 

During the early stage the nuclei stain 
faintly and is of homogenous appear- 
ance. The cell disintegrates. The 
striations disappear in the muscles. 
All other cells in area suffer the fate 
~- of the fixed tissues, 



46 PATHOLOGY. 

Pathologic Physiology. 

It is supposed to be due to the union 
of the dying cell protoplasm with the 
fibrinogen of the blood. 

Many chemicals may act direct. 

Bacterial products may act fibrino- 
genetically. A coagulated area may 
be cast off by ulceration, or it may 
become liquified, caseated, suppurated, 
encysted and dissolved or reabsorbed. 

It may finally be converted into scar 
tissue. Function is more or less com- 
pletely lost. 

b. Liquefaction Necrosis or Colliquefac- 
tion is the death of tissue with lique- 
faction. It is divided into— 
Primary liquefaction necrosis, as seen 

frequently in the central nervous sys- 
tem, where it follows pathologic con- 
ditions which elsewhere would pro- 
duce coagulation. 

Secondary liquefaction necrosis is a 
form in which the areas of coagula- 
tion necrosis, cheesy necrosis, inflam- 
mation, gangrenous tissue and tumors 
may become liquefied. 
Pathologic Anatomy. 
Early stage is softer than normal tis- 
sue. The fibrillar tissue begins to dis- 
solve and the area becomes filled with 
a liquid the consistency of which de- 
pends upon the tissue involved. The 
cells are variously degenerated, and 
after a while nothing but detritus re- 
mains. In some cases the exudate may 
coagulate. The color may be white 
from emulsified fats; yellow from pig- 
ments and fat; red or brown from 
blood pigments, or deeply colored from 
bile pigments. Liquefactive areas may 
be discharged, coagulated, reabsorbed, 
encysted or organized. 

c. Caseation is where coagulation ne- 
crosis takes on a cheese-like appear- 
ance. It is typical of tuberculosis and 
syphilis. It is secondary to coagula- 
tion necrosis. It results from the ne- 
crobiotic effects of the tubercle bacillus 
or the poison of syphilis upon the 
tubercle or gumma. 

Microscopically. The nuclei disappear 
and the cells break down into a struct 
tureless, cheesy mass. 



GANGRENE. 47 

Caseated areas may be cast off, reab- 
sorbed, encysted or calcified. 

d. Fat Necrosis designates a peculiar 
type of necrosis, which occurs in very 
stout people, over small areas in the 
normal fat. It is quite distinct from 
ordinary fatty metamorphosis. 

It is seen in the abdominal walls and the 
subperitoneal fat. 

The affected areas are usually not larger 
in size than a pea, soft or gritty and 
white in color. The area may be sur- 
rounded by inflammation. 

Microscopically. The cells lose their 
transparency, though they still stain 
with osmic acid. 

There is no agreement as to the cause of 
this condition. Some contend that it is 
due to fat splitting ferment of pan- 
creatic secretion. 

The necrotic portions when not infected 
may be absorbed or organized, fol- 
lowed by a cicatrix, or may become 
calcified. The liquefied portion may be- 
come encapsulated and remain as a 
cyst. 

e. Gangrene is the putrefaction of areas 
of necrosis. It may be classed as — 

1. Primary, when a particular bac- 
terium produces a direct gangrenous 
result, as in malignant oedema, 
anthrax, etc. 

2. Secondary, when saprophytic bac- 
teria decompose an area already 
dead. 

Gangrene may be divided into — 

1. Dry gangrene* due to — 

a. Arterial disturbance or occlusion 
result of arterial obstruction of se- 
nility, arterial embolism or throm- 
bosis, freezing, ergotism, Ray- 
naud's disease. 

b. The moist type, when putrefaction 
is slow and the fluids evaporate. 

Dry gangrene is circumscribed and 
ends in mummification. The color 
is dark or black. Early the color 
may be yellow or brown. There is 
little toxic absorbtion in this type. 

2. Moist gangrene generally results 
from extensive venous occlusion. fc In 
some cases it may be due to arterial 



48 PATHOLOGY. 

occlusion. 
Causes. 

a. Internal emboli, as in pulmonary 
arteries and veins. 

b. In the lungs as the result of in- 
spiratory pneumonia, abscesses, 
neoplasms, bronchiectasis and in 
diabetes. 

C. Traumatism and pressure con- 
tusions, as seen in intussusception 
and strangulation of bowels; very 
frequent in vermiform appendix; 
also as result of torsion in mov- 
able kidneys, spleen or tumors. 

d. Infections. 

e. Skin disease (rare). 

f. Severe trophic lesions, as decu- 
bitus, etc. 

Pathologic Anatomy. 

Macroscopically. The consistency 
of part becomes softer. There is 
local or widespread emphysema. 
The color is dark brown. The 
skin is black and covered with 
fciebs. 

Coagulation necrosis or an inflam- 
matory zone may surround the 
areas, the latter producing a line 
of demarkation. In some cases, 
as in the diabetic, neither zone is 
formed. 

Microscopically all the cells of the 
tissue are involved. The cells are 
the first to succumb. Hemorrhages 
into the area are common. The 
connective tissue and elastic fibers 
are liquefied. 

The affected areas contain crystals 
of pigment, fatty acids, cholestern, 
leucin, tyrosin, phosphates and 
carbonates, ammonia and fatty 
acids, indol and skatol, amins, 
sulphurated hydrogen, carbonic 
acid and other gases give rise to 
pronounced odors. There is more 

. or less toxic absorbtion. 

Pathologic Physiology. 

The condition may progress and 
cause death, or it may become 
circumscribed. 

In the. circumscribed a line of de- 
markation is formed by inflamma- 
tory reaction. The mass is cast 



INFLAMMATION. 49 

off if the area is superficial or 
encysted if area is internal, which 
is then followed by reabsorbtion 
of the contents and calcification 
of the sac. 

In dry and vascular form of moist 
the gangrene is generally limited. 
In the other forms it is progres- 
sive. 

From the above you will note then 
that gangrene is circumscribed, 
progressive or metastatic. 

INFLAMMATION AND REGENER- 
ATION. 

1. INFLAMMATION is the reaction which 
occurs in tissues to various forms of 
irritations, and is characterized by the 
cardinal symptoms of heat (calor), red- 
ness (rubor), pain (dolor), swelling 
(tumor) and later altered function 
(functio laesae). 
Etiology. Irritation by — 

1. Mechanical, as in fractures and 
wounds. 

2. Chemical, as by strong acids. 

3. Electrical. 

4. Thermal or opposite, burns and frost 
bites. 

5. Microorganisms. 

6. Metabolic, as in gout, etc. 

7. Mental, as in hyponosis, etc. 
Phenomena of Inflammation. 

1. Vascular changes. 

a. Momentary contraction of the ar- 
teries. This is probably reflex and 
is rarely observed. 

b. Dilitation of arteries, due in part 
to nervous reflex, but probably 
most to some degeneration of ves- 
sel walls. The blood courses more 
quickly at first and is then followed 
by a slowing of the blood current, 
with sometimes complete stoppage 
(stasis), brought about by the dam- 
aged endothelial cells, , which swell, 
increase in adhesiveness, . thus en- 
croaching upon the lumen of the 
vessel. This condition ' is followed 
by— 

2. Exudative changes. 

a. Leucocytes in r . the. plasmatic, zone 



50 PATHOLOGY. 

of the blood stream increase in 
number and cling to the vessel 
wall. 
b. Leukocytic migration through the 
vessel wall to the outside and into 
the tissues. This is brought about 
by- 

1. The leucocytes' own ameboid 
movement. 

2. Chemotoxis (positive), the attrac- 
tive chemical influence at the site 
of irritation. 

3. Increased permeability of the 
vessel wall and blood pressure 
aid to a minor extent. 

Coincidentally with migration there 
is — 
C. Exudation of altered blood plasma. 
The amount and character of which 
varies with the nature and condi- 
tion of the tissues affected and the 
character of the irritant. 
The exudate is relatively rich in al- 
bumen and more coagulable than 
dropsical fluid. 
d. Diapedesis of Red corpuscle. 

The escape of the red corpuscle 
from the capillaries is a passive 
process, being due to blood pressure. 
It is most marked when stasis has 
occurred. 
3. Proliferative changes. Some authori- 
ties hold that proliferative changes 
are not in reality a part of inflam- 
mation, but are for the purpose of 
tissue repair after inflammation. It 
will, however, be regarded as a part 
of inflammation. 
In the inflammed area, especially at the 
periphery, the tissue is infiltrated with 
round cells resembling lymphocytes, 
or mononuclear leucocytes frequently 
showing evidences of karyokinesis. 
They are derived from fixed connec- 
tive tissue cells and the endothelia of 
lymph spaces. 
The newly formed connective tissue cell 
becomes in part wandering and more 
or less phagocytic in nature, and in 
part fixed, and assumes a regenera- 
tive role, frequently called flbro-blastic 
cells. The appearance of the tissue at 




Fig. 5. Acute appendicitis, with ex- 
tensive round cell infiltration of all the 
coats of the appendix. 




Fig-. 6. Fibroblasts forming- fibrous 
tissue. (Ziegler.) 




m 



Fig. 7. Chronic interstitial nephritis; 
great increase of connective tissue 
around the glomeruli, renal tubules and 
blood vessels; from a case of arterio- 
capillary fibrosis. 



INFLAMMATION. 51 

this stage is characteristic and is 
termed Round-cell infiltration. 

Granulation Tissue. 

Active proliferative changes, multipli- 
cation of new blood vessels, pre-ex- 
isting vessels endothelial outgrowth, 
all surrounded by various forms of 
round cells constitute granulation tis- 
sue. It is frequently seen in the floor 
or ulcers. It is more properly a re- 
generation. 

4. Degenerative changes. 

The nature of the degeneration de- 
pends upon the severity of the irri- 
tation. Very powerful irritants cause 
necrosis at once. Irritants which 
merely disorder but do not entirely 
destroy the cells are apt to cause in- 
flammation. 

The degenerative changes may be 
physiologic or there may be structural 
changes such as cloudy swelling, 
mucoid degernation, liquefaction, fat- 
ty or coagulation necrosis. These de- 
generations though primary are often 
followed by a secondary degeneration 
which may serve to spread and in- 
tensity the original inflammation. 
Varieties of inflammation. 

a. Catarrhal, mucous inflammation or 
catarrh, occurs on the mucous mem- 
branes, as in the nose, throat, 
bronchi, stomach, bowels, etc. 

The mucosa is congested, a serous ex- 
udation is discharged from the sur- 
face, and to some extent it is re- 
tained in the tissue causing edemat- 
ous swellings. Tne mucous glands 
increase their secretion and leucocytes 
escape. When abundant, as in nasal 
catarrh, the process may be purulent 
or suppurative, more frequently 
mucopurulent. 

When inflammation is chronic there 
is considerable productive inflam- 
mation with consequent irregular- 
thickening or thinning of area in- 
volved. 

b. Serous Inflammation, is character- 
ized by an abundant exudate of 
serum with very little cellular 
matter. It is frequently seen in 
pleural or peritonitic effusions and 



52 PATHOLOGY. 

as edema of the larynx, etc. 
All serous effusions are not inflam- 
matory. 

Some are purely mechanical, as in 
dropsies. 

Inflammatory effusions differ from 
dropsical in that they contain more 
albumin and fibrin. 

C. Fibrinous (croupous) Inflammation, 

is characterized by a thick deposit of 
fibrin and occurs on the serous sur- 
faces as in peritonitis, larynx and 
bronchi in acute infections as in ty- 
phoid, small-pox and pyaemia and in 
the lung in pneumonia. 
The term sero-fibrinous is applied 
when it is associated with serous 
exudation and fibrino-purulent when 
exudate is purulent. 

d. Diphtheric Inflammation, is of the 
same nature as the fibrinous but diff- 
ers in that it is much more severe and 
having associated with the coagu- 
lated exudate a necrosis of the cells 
of the part involved. It is typically 
seen in diphtheria but may also be 
seen in other conditions. 

The membrane consists of a net- 
work of fibrin or fibrin masses en- 
closing degenerated epithelial cells 
and emigrated leucocytes. 

e. Supperative Inflammation, although 
generally caused by infection with 
pyogenic micro organisms, it has also 
been produced by calomel, croton oil, 
turpentine, etc. It is characterized 
by an abundance of emigrated leu- 
cocytes and the tendency to liquefac- 
tion. 

The most common bacteria producing 
it are the pyogenic staphylococci and 
streptococci but other forms not gen- 
erally considered pathogenic may 
also cause it, as the typhoid and coli 
bacillus, gonococcus and others. 
Bacteria entering the tissue by means 
of the blood or otherwise, first cause 
degeneration or necrosis, congestion 
follows with exudation of leucocytes 
and plasma and more or less fibrin 
formation and finally softening of the 
whole area involved from the action 
of the bacteria on the cells, creating 
a ferment. 



INFLAMMATION. 53 

The packed exudative cells and the 
pressure together with the local 
anemia produced are additional fac- 
tors that lead to degenerative changes 
and pus-formation. The fluid exudate 
fails to coagulate and form fibrin. 

Pus consists of a liquid part (liquor 
puris) and a corpuscular part. 

The liquid part is made up of a less 
coagulable blood plasma containing 
quantities of albumose. 

The corpuscles are chiefly more or 
less degenerated polymorphonuclear 
leucocytes. 

When the suppuration within a tis- 
sue or organ is circumscribed it is 
called an, — 

Abscess. The tissues surrounding 
the area show proliferative changes, 
forming a sort of retaining wall. In 
slow forming abscesses the wall is 
quite firm and is often called pyogenic 
membrane. 

The abscesses will soften the tissues 
in the direction of least resistance and 
discharge their contents onto the sur- 
face by sinuses. 

The pus may become inspissated by 
the absorbtion of the liquid part, the 
remaining matter undergoing various 
degenerations. The membrane may 
become organized and thus encap- 
sulate the abscess. 

Ulcer. An ulcer is of the same con- 
struction as an abscess except that 
it appears with erosion upon the skin 
or mucous surfaces. 
Suppuration of the skin and sub- 
cutaneous tissues are localized or 
diffused. Of the localized we have 
pustules, furuncles and carbuncles. 

f. Parenchymatous Inflammation is a 
term applied to inflammations when 
it attacks the proper tissues of an 
organ as in nephritis and leads to 
degeneration of its active cells. 

g. Productive Inflammation. 

The term intestitial inflammation is 
applied to this form in contradistinc- 
tion to the parenchymatous form. 
The proliferative changes predominate 
over exudation and degeneration. 



54 PATHOLOGY. 

When the inflammation becomes 
chronic the proliferative changes in 
the tissue predominate more or less. 
There is essentially some primary de- 
struction of tissue so that productive 
process must therefore be regarded 
as reactive. 

Repair of Wounds. This is brought 
about by productive inflammation. 
Where there is but little exudation 
and proliferated connective tissue 
cells, it is called healing by immedi- 
ate union. This is when the lips of 
the wound are clean and carefully 
drawn together at once. 
Where opposition is slightly delayed 
or less accurate, the exudation is 
greater, and the healing is more slow, 
it is called healing by first intention. 
If the wound is exposed or irritated 
there will be seen, after 48 hours, 
small red elevations (granulations) 
made up of newly formed loops of 
capillaries covered with round cells 
and later there may be giant cells. 
The round cells elongate and form 
fibrous tissue which contracts and 
forms ciratrices or scars. 
The continuity is re-established by 
old epithelial cell multiplication at the 
edges of the wound. This is called 
healing by granulation or second in- 
tention. 

Adhesions. The formation of ad- 
hesions following inflammation of 
serous surfaces, is brought about by 
the fibriuous primary exudation which 
causes agglutination of the neighbor- 
ing surfaces and is then followed by 
conditions somewhat similar to the 
healing of wounds. 

Repeated attacks of the parenchyna- 
tous inflammation results in an in- 
terstitial inflammation in which the 
supporting framework of the organ is 
involved. This connective tissue over- 
growth results in cirrhosis, fibrosis or 
induration of the organ. 

General Fibrosis is a tendency to wide 
spread productive inflammation, sup- 
posedly due to alcoholic, gouty,. syphil- 
ic, etc. intoxications It affects the 
blood vessels especially, also the 
liver (cirrhosis), kidney (interstitial 



REGENERATION. 55 

nephritis), etc. 

This form of inflammation may also 
attack the epithelia of the skin, 
mucous membranes adenoid tissues, 
cartilages, bones or the periosteum. 
h. Hemorrhagic Inflammation, is an in- 
flammation in which the exudate is 
usually rich in red corpuscles. It is 
distinguished from ordinary inflam- 
mation in which hemorrhages occur 
accidentally. 

The cause is probably due to the ir- 
ritating cause falling principally on 
the blood vessels or that the patient is 
suffering from cancer, tuberculosis, 
hemophilia, etc. 

Purulent inflammation is generally 
caused by infection with microorgan- 
isms. 

Resolution. 

Where exudation is small, the emi- 
grated leucocytyes and the liquid ex- 
udate re-enter the blood current or 
escape through the lymphatics. The 
connective tissue cells remain or be- 
come wandering cells. 
When the exudate is abundant, the 
liquid element is removed by the 
blood or the lymphatics, but the cells 
first degenerate and are emulsified, 
then gradually absorbed. 
In purulent inflammation the pus is 
discharged through openings, extern- 
ally or into the cavities of the body, or 
may be inspisated. 

If the inflammation of the parench- 
yma may recover if the degeneration 
is not too severe, or may be softened 
and removed. 
II. REGENERATION is the formation of 
new cells or tissues to take the place 
of those destroyed. It may be divided 
into — 

1. Physiologic. Occurs in the normal 
organism, counterbalancing the cel- 
lular wear and tear. 

The cells multiply, but do not go be- 
yond the point of normal develop- 
ment. Some unknown restraining in- 
fluence prohibits the cells from go- 
ing beyond their limit. The repro- 
ductive process is probably depend- 
ent upon the loss of substance. 



56 PATHOLOGY. 

Where the normal restraining influ- 
ence is deficient giant growth results. 

In normal regeneration the process is 
one of gradual cell multiplication. 

Cell multiplication or division occurs 
in two vva>s, i. e., it takes place 
directly by cleavage (amitosis), which 
seldom takes place, or by the indi- 
rect method (karyokinesis), which is 
the usual method. 

2. Pathologic Regeneration is a mas- 
sive and often atypical reconstruc- 
tion that follows disease or injuries. 

In this form there seems to be an ab- 
normal stimulation of the reproduc- 
tion of cells as well as a reduced re- 
straining influence. 

Various toxic substances probably stim- 
ulate the formative process, though 
in regeneration following mechanical, 
thermal or toxic causes there is first 
a destruction of cells. The regenera- 
tion which follows may be due to 
relief from accustomed pressure, 
which may serve to withdraw the re- 
straining influence. 

Regeneration is the more or less ef- 
fective effort of nature to replace in- 
jured or excised tissue. The com- 
pleteness of the restoration is in the 
proportion to the tissues lack in 
higher organization and differentia- 
tion. 

The lower the type of tissue and the 
younger the individual the more com- 
plete the restoration. 

Organization is the method by which a 
non-infective organic foreign body is 
absorbed and replaced by connective 
tissue. It is best seen in thrombi and 
in small tissues killed by infarcts. 

In a clot the endothelium of the vessels 
proliferate to form fibroblasts, new 
vessels from the vasa vasorum grow 
into the lumen, and with the increase 
of the young connective tissue there 
is a disappearance of the clot. 

The same process takes place in an 
infarct. The new vessels and fibro- 
blasts are furnished from the vessels 
and the cells around. 

Metaplasia is the transformation of one 
form of tissue into another without 



HYPERTROPHY. 57 

any intervening stage of regeneration 
by cellular multiplication. The change 
may be a transformation of the inter- 
cellular substance, as when common 
connective tissue is converted into 
myxomatous tissue or the fibrillar 
into cartilaginous or bony tissue. 

The tissue never changes its species, 
and the character once altered is 
permanent. 

PROGRESSIVE TISSUE CHANGES. 

. HYPERTROPHY. Is the increase in 
size of the tissue elements without 
marked alteration from the normal 
structure. 
Causes. 

1. Increase of functional demand, as in 
hypertrophy of the muscles of ath- 
letes; hypertrophy of a limb after in- 
jury to the opposite limb; hypertro- 
phy of a kidney after disease or re- 
moval of its fellow. 

2. Disturbances of the nervous sys- 
tem. 

3. Continued congestion, though this is 
the means in which it is affected 
rather than the original cause. 
Pathologic Anatomy. 

The parts are uniformly increased 

in size. 
Histologically, hypertrophy may be 

divided into — 

1. Simple or true hypertrophy, in 

which there is an increase in 
the size of the individual cells. 
This is seen in the uterus dur- 
ing pregnancy. 

2. Numerical hypertrophy or hy- 
perplasia. In this form the cells 
are of the normal size, but are 
increased in number. This is a 
common factor in hypertrophy. 
It may be limited to one tissue 
of an organ, principally the con- 
nective tissue. 

There are all grades between the 
extremes. Some cases are des- 
ignated clinically as — 

Hypertrophic enlargement, which 
is a hyperplasia of the connec- 
tive tissue, with a tendency to 



58 PATHOLOGY. 

atrophy of the organs proper 
substance, as in hypertrophic 
cirrhosis of the liver, etc. 
Pathologic Physiology. 

When there is an increased de- 
mand upon an organ by reason of 
disease in itself or in a related 
organ, or from loss of a correlated 
organ, the organ undergoes com- 
pensatory hypertrophy. This is seen 
in the kidney when the other is 
diseased or absent; in the heart in 
valvular disease, and in the en- 
larged muscles of laborers. 

II. TUMORS. New Growths, Neoplasms, 
Pseudoplasm. 

A tumor is a growth which consists 
of a non- inflammatory mass of cells 
atypical in structure and arrangement 
and grows at the expense of the 
body. 

Causes. There are several theories, 
none clear. 

1. "Cell Rests" (Cohnheim's theory) or 
defective development. This theory 
is based upon frequent small errors 
of development, which would lead to 
a misplacement of portions of the 
blastoderm in the tissues, derived 
from a different layer of the em- 
bryo. These cell rests differ in func- 
tion to the part in which they lie, 
and are therefore liable to sprout 
when subjected to irritation or their 
vitality stimulated, with the conse- 
quent formation of tumors. 

2. Irritation or injuries (Virchow's 
theory), as seen in epithelioma of 
chimney sweeps and pipe smokers 
and carcinoma of breasts, etc. 

3. Infectious character has been con- 
sidered by some authorities as a 
cause, in that in certain respects 
some tumors resemble infectious 
processes in their effect upon the 
general health and their tendency to 
metastasis. 

Other investigators have determined 
that no ordinary bacterium play any 
causative part. The possibility of 
• ultra- microscopic organisms has been 
considered. Secondary and accidental 
invasions of • bacteria . into tumors 



TUMORS. 59 

may occur and lead to confusion. 
The transplantation of tumors from 
one part to another does not differ 
from ordinary metastasis. It, how- 
ever, proves only the proliferative 
tendency of the cells of the growth 
and not the infectious origin. 

4, Anaplastic. In this theory the tumor 
results from a retrograde change in 
the vital properties of cells so that 
they tend toward the characteristics 
of the germ- cells and multiply in an 
indeterminate manner. 

5, Parasites (coccidia) have been de- 
scribed as occurring in cancer, but 
this still awaits proof. 

A late theory is that the cancer cell 
does not spring from pre-existing 
epithelium, but is a parasite from 
without. 

Predisposing causes play an important 
part in the formation of a new 
growth. We have therefore — 

1. Constitutional predisposition from — 

a. Advanced age. 

b. Lowered vitality from disease, 
etc. 

2. Family predisposition, formerly re- 
garded of great importance, was 

probably over-estimated, but can- 
not entirely be denied. 
Structure of Tumors 

1. Tumors conform more or less with 
structure of some one or more tis- 
sues. 

2. Tumor cells represent some one of 
several types of normal cells. They 
differ from normal cell in that — 

a. They may be smaller or larger. 

b. They may be embryonic or un- 
developed. 

c. They may be asynametrical or 
abnormal in mitosis. 

d. Inclused leucocytes are often 
found in tumor cells and have 
frequently been mistaken for 
parasites. 

e. In the malignant tumor cell there 
is not the normal number of 
chromosomes. 

3. Arrangement of tumor cells differ 
from that of normal, tissue, in that — 



60 PATHOLOGY. 

a. The orderly arrangement of cells 
and stroma or the intercellular sub- 
stance is wanting. 

b. Scattered through the stroma and 
between the tumor cells are vari- 
ous forms of leucocytes. 

4. Blood vessels of tumor have poorly 
developed walls, which permits ready 
emigration of leucocytes. 

5. Regenerative changes is constantly 
seen in the formation of the connec- 
tive tissue frame work. 

Shape of tumors. This depends upon 
the situation, growth and influence 
of the surrounding parts. They may 
be divided into — 

1. Circumscribed growths, which may 
be of various shape, but distinguished 
by a line of demarkation and often a 
capsule. 

They usually grow in an expansive 
manner from the center, pushing the 
older parts toward the surrounding 
tissue. 

According to the appearance of the 
growth the terms miliary, tubercular, 
nodular are employed to designate the 
grades when the tumor is buried in 
the tissue or project more or less 
from the surface. When the growth 
has a constricted base the term 
fungiform is used. When it is at- 
tached by a narrow pedicle the term 
polypoid is used. Wart-like growths 
are called verucose or papillary. 
Cauliflower growths are called den- 
dritic. 

2. Infiltrating growths are those in 
which there is no distinct line of de- 
markation, and the extent of tissue 
involvment cannot be definitely de- 
termined. 

The growth is irregular. Parts of the 
periphery or original growth may ex- 
tend, or secondary nodules may form 
in the neighborhood, afterwards be- 
coming confluent with the original 
mass. 

Pathologic Physiology. 

Tumors may be said to be parasitic, 
in that they live at the expense of 
the organism. 



TUMORS. 61 

Tumors may be classed as — 

1. Benign, when it does not apparently 
affect the health. They are danger- 
ous by reason of the pressure to vital 
parts or the secondary changes to 
which they are liable. 

2. Malignant, when it shortens life. 
It infiltrates the surrounding tissue. 
It tends to recur after removal. 

It spreads to distant organs by the 
blood vessels and lymphatics (Metas- 
tasis), or transplantation of a tumor 
from one part of the body to another. 

A specific poison is formed by the 
tumor cell, which disturbs the health 
from the first, and the patient shows 
a peculiar, sallow complexion know-n 
as a cachexia. 

Tumors w T hich are ordinarily benign 
may recur after operation or cause 
metastasis, the terms — 

1. Primary tumors refer to the orig- 
inal tumor and the number. They 
are generally solitary, though they 
may be multiple, as in carcinoma, 
appearing in both breasts simul- 
taneously or in other different parts 
of the body. 

Benign tumors are usually solitary. 

2. Secondary tumors refer to meta- 
static growths and are usually mul- 
tiple. 

Classification of Tumors. There is no sat- 
isfactory classification. The classifica- 
tion by Ada mi is given below — 

I. Blastomata, composed of products of 
aberrant growth of cells and tissues of 
the individual in whom they are de- 
veloped. 

Adult tissues may be divided into two 
types — 

1. Lepidic tissue (rind or membrane), 
tissue in which there is no stroma 
with blood and lymph vessels be- 
tween the individual cells. 

2. Hylic or pulp tissues (crude matter, 
supporting or packing tissue), tissue 
in which there is homogenous , or 
fibrillated inter-cellular substance 
separating the specific cells. 

Both of these types are derived from 
the epiblastic, mesoblastic and hy- 



62 PATHOLOGY. 

poblastic layers of the embryo. 
They are derived from the — 

a. Epiblast. 

1. Lepidic. Skin and its glands, 
portions of eye, ear and brain, 
etc. 

2 Hylic Nerve and glia cells. 

b. Hypoblast. 

1. Lepidic. Epithelium of the di- 
gestive tract and associated 
glands. 

2. Hylic. Intervertebral disc (noto- 
chord). 

c. Mesoblast. 

1. Lepidic. 

a. Mesothelium — lining of pleura, 
pericardium, specific cell of 
suprarenals, kidneys, testis, 
ovary, epithelium of uterus, 
fallopian tubes, vagina, vas 
deferns, etc. 

b. Endothelium — lining of the 
blood vessels and lymphatics. 

2. Hylic. 

a. Mesenchyme — connective tis- 
sue, bone, marrow, etc. 

b. Mesothelium — striated muscle. 
Inasmuch as both hylic and lepidic tissue 

is found in all three layers, blastomata 
may be classified both embryologically 
and hystologically into — 
1. Lepidomata or "Rind" Tumors, 
a. Primary Lepidomata. 

1. Epilepidomata are overgrowth of 
tissue derived from epiblastic lin- 
ing membranes or true epiblast. 

a. Typical. Papilloma, epidermal 
adenomata (of sweat, salivary, 
sebaceous and mammary glands, 
etc.). 

b. Atypical. Carcinoma develop- 
ing in the same organs and re- 
regions. 

2. Hypolepidomata. 

a. Typical. Adenoma and papil- 
loma of the digestive and re- 
spiratory tract, thyroid, pan- 
creas, liver, bladder, etc. 

b. Atypical. Carcinoma develop- 
ing in the same organs and re- 
gions. 



TUMORS. 63 

b. Secondary Lepidomata. Tumors 
whose characteristic constituents 
are cells derived in direct descent 
from the persistent mesothelium of 
of the embryo. 

1. Mesolepidomata. 

a. Typical. Adenoma of kidney, 
testicle, ovary, urogenital ducts; 
adenoma of uterus and prostate; 
adenomas originating from se- 
rous membranes, "mesotheli- 
oma" of pleura, peritoneum, 
etc. 

b. Atypical. Cancer of the above 
mentioned organs, squamous 
endothelioma, so-called, of se- 
rous surfaces, epithelioma of 
vagina. 

2. Endothelial Lepidomata. Tumors 
originating from endothelium of 
blood and lymph vessels; endothe- 
lioma, perithelioma. 

1. 2. Hylomata or "Pulp" Tumors. 

a. Epibryiomata. Tumors whose char- 
acteristic constituents are over- 
growths of tissue, derived from the 
embryonic pulp of epiblastic origin. 

1. Typical. True neuroma, glioma. 

2. Atypical. Gliosarcoma. 

b. Hypohylomata. Tumors derived 
similarly from the embryonic pulp 
of hypoblastic origin. Chordoma. 

c. Mesohylomata. 

1. Mesenchymal Hylomata. Derived 
from tissues originating from the 
persistent mesoblastic pulp or 
mesenchyme. 

a. Typical. Fibroma, lipoma, 
chondroma, osteoma, myxoma, 
leiomyoma. 

b. Atypical. Sarcoma. Derived 
from mesenchymatous tissues 
with its various subdivisions, 
nbrosaroma. spindle cell sar- 
coma, oat-shaped cell sarcoma, 
chondrosarcoma, osteosarcoma, 
myxosarcoma, melanotic sar- 
coma, etc. 

2. Mesothelial Hylomata. Tumors 
which are overgrowths similarly 
of tissues derived from embryonic 
pulp of definitely mesothelial 
origin. 



64 PATHOLOGY. 

Rhabron^oma. 
The Histology and the Distribution of the 
Blastomata. 

1. Fibromata are benign connective tis- 
sue growths, consisting chiefly of fibers 
with cells, which become more nu- 
merous in proportion to the rapidity 
with which the tumor grows. The 
growth is usually exceedingly slow. 
They are destructive only in so far as 
they are capable of producing mechan- 
ical injury by pressure. 

In some cases they will recur after re- 
moval, and in these instances resemble 
sarcoma. 

a. Hard Fibroma is a dense, tendon 
like formation, having only a few 
cells and flat fibers. It is often en- 
capsulated. It is seen in the perios- 
teum, particularly of the dental 
alveoli. 

b. Soft Fibroma is of a soft consistency 
and of a loose texture. It is seen as 
a non-capsulated tumor of the skin. 
Also as polypi of the nose. 

c. Elephantoid Fibromata (mimic ele- 
phantiasis), multiple tumors of the 
skin. 

d. Fibroma Moliuscum (M. non-con- 
tagiosum) is absolutely different from 
M. contagiosum. It is made up of a 
great number of small fibromata 
growing from the skin and are sessile 
and pedunculated. Microscopically, it 
is shown to be made up of both loose 
and dense fibrous tissue. 

e. Cheloid is a dense, fibrous growth, 
appearing usually, but not always, 
in cicatrices, and is of the same 
structure. It may assume a sarco- 
matous character. 

f. Psammoma, or brain sand tumor, is 
found in the pineal gland, in the 
choroid plexus and the dura mater. 
It is a soft connective tissue, new 
growth, infiltrated with calcareous 
globes and spicules. 

The fibromata also include many 
tumors which have been called neu- 
romata because they spring from the 
nerve sheaths. There is, however, no 
nervous tissue to be found in their 



TUMORS. 65 

structure. 
Seats. Always springing from pre-ex- 
isting connective tissue. They are 
found in the subcutaneous connective 
tissue, submucous tissue, periosteum, 
tendons and tendon sheaths, and the 
fibrous covering of the nerves. The 
uterus, ovaries, kidneys and heart 
muscle, serous membranes of the 
chest and abdomen and the central 
nervous system. 

2. Myxoma, is a tumor made up of stel- 
late or spindle-shaped, connective tissue 
cells and an inter-cellular substance 
containing a mucoid material. Mucoid 
tissue is physiologically present in the 
umbilical cord, the foetal subcutaneous 
tissue and the vitrious of the eye. 

The tumor is soft, flabby and rounded in 
structure. It is surrounded by a cap- 
sule. It may sometimes be lobulated, 
or it may be diffuse, having no capsule. 
Found in the subcutaneous and sub- 
mucous tissue and the connective tissue 
of certain organs, principally the mam- 
mary gland along the course of nerves, 
brain and the spinal cord. It may also 
be found in the subserous tissue. It is 
usually found alone, but may be asso- 
ciated with or as a degeneration of 
lipoma, fibroma, chondroma and ade- 
noma, the prefix Myxo being used with 
each of these terms. 

The myxoma is benign, but it may be 
myxosarcomatous. 

3. Lipoma is a tumor made up of fat 
tissue, which does not differ greatly 
from the normal subcutaneous fatty 
tissue. It resembles greatly the ap- 
pendices epiploicae. 

The tumor cells are frequently larger 
and contain more oil than the normal 
fat cell. 

The tumor is soft to the feel unless it is 
made tense by fibrous trabeculae run- 
ning in from its capsule, it is then 
called a flbrolipoma. 

The capsule may be wanting in some 
cases, the tumor being then diffuse. 

The tumor may be solitary or multiple. 
Congenital lipoma are not rare, but it 
generally appears during adult years or 
middle life. 



66 PATHOLOGY. 

It is benign and of slow growth and 
usually occurs in the subcutaneous 
fatty tissue of the back, shoulders, 
buttocks or limbs, the submucous and 
the subserous tissue. 

The mammary gland and kidneys are the 
most frequent seats in the organs of 
the body. 

4. Xanthoma is a benign tumor made up 
of modified fatty tissue resembling em- 
bryonic adipose tissue, with more or 
less round cell infiltration. 

a. Xanthoma vulgare occurs frequently 
in or near the eyelids in the form of 
yellow, flat elevations. 

b. Xanthoma diabeticorum is found in 
diabetic patients. It is similar to the 
above, but is more inflammatory and 
rarely affects the eyelids or the face. 

5. Chondroma is a tumor composed of 
cartilage. It consists of distinct 
forms, which differ somewhat in ap- 
pearance. 

a. Ecchondromata, or cartilagenous 
outgrowths, spring from the cartilage 
and appear as irregular outgrowths, 
or may be wart-like in form, or may 
occur in rows or groups. They may 
be loosely or firmly attached, and are 
seen in rheumatoid arthrites, where 
they may become detached, or they 
may be seen on the surfaces of the 
costal or laryngeal cartilages, where 
they are firmly attached. 

b. Enchondromata, cartilageous tumors 
or chrondromata proper, are the 
more common form and begins in 
some other form of connective tissue. 

They occur in bones or the periosteum 
and have a rounded or lobular ap- 
pearance. 

Chondromata, in all probability, arise 
from "cell rests," and are unexpect- 
edly found to occur in the parotid- 
gland and in the testicle. 

Enchondroses occurs in the neighbor- 
hood of bones, in muscles and ten- 
dons and in organs mentioned above. 

The ecchondroses are most frequently 
found about the long bones, partic- 
ularly at their epiphyseal attachment. 

All forms are hard, though secondary 



TUMORS. 67 

softening may occur. Associated mu- 
cous, sarcomatous or other softer tis- 
sue will regulate its consistency. 

Histologically, the cartilage cells are 
found inclosed in a hyaline or fibrous 
matrix. The cells are frequently with- 
out a capsule and not regularly ar- 
ranged. The inter-cellular substance, 
which is abundant, is frequently gela- 
tinous, mucoid or fibrous. 

When the tumor is associated with 
myxoma and sarcoma the structure 
varies. They are then called mixed 
tumors. When there is calcification 
and true ossification it is called os- 
teochondroma. 

Osteoid chondroma is the name given 
to it when the inter- cellular substance 
suggests bone structure, but actual 
ossification has not occurred. 

The tumor is usually benign. 

Metastasis may occur. 

6. Osteoma is a tumor composed of os- 
seous tissue. The pathologic growth 
of bone is seen as a senile change, and 
also results from chronic irritation and 
inflammation, as seen in the deltoid 
muscle, from carrying a rifle, and around 
inflamed joints. Osteoma is closely 
allied to the chondroma and, like the 
chondromata, two forms are distin- 
guished. 

a. Exostoses and osteophytes are out- 
growths differing in shape and ap- 
pearance only. The exostosis is a di- 
rect outgrowth from bone of a more 
or less warty character. 

The osteophytes are extensive, bony 
deposits upon bones and are less 
closely attached. They are formed 
either of spongy or compact bone. 
When spongy, it grows from the 
epiphyseal cartilage. When compact, 
it grows from and beneath the perios- 
teum. 

They are divided into— 

1. Ostoma durum, hard. 

2. Osteoma spongiosum, soft. 

3. Osteoma eburueum, when exceed- 
ingly dense. 

When arising and consisting of den- 
tine it is known as odontoma. 

b. Enostoses (osteoma proper or hetro- 



68 PATHOLOGY. 

plastic osteomata) are those which 
are separated from the bone, as when 
they appear in the medullary canal 
and in the serous membranes. 
Osteoma are found in connection with 
bone, cartilage or the connective tis- 
sue near bone. 

They are sometimes found in other 
connective tissues, serous membranes 
or organs as testicles and the parotid 
gland. 

The growth is benign. Secondary de- 
generations may occur and are some- 
times associated with other tumors, 
such as chondroma, myxoma, fibroma 
and sarcoma. 

7. Myoma is a tumor composed of mus- 
cular tissue. 
It is divided into — 

a. Leiomyoma or Myoma laevicellulare 
is made up of unstriated muscle 
fibers running in various directions. 
There is generally some fibrous tissue 
associated with it. If cut transversely 
there may or may not be a round 
nucleus, depending upon where the 
cell is cut. 

If cut longitudinally a rod-shaped 
nucleus will be seen, the spindle out- 
line of the cell may be indistinct. 

There is a distinct capsule to the 
tumor. 

Its chief seat is in the uterus and its 
apendages, though frequently it oc- 
curs in the prostate and alimentary 
tract. Rarely it is found in the walls 
of blood vessels, the nipple and the 
skin. 

The tubercula dolorosa (Wood's tumor) 
of the skin is a myoma probably de- 
rived from the arrector pili muscle. 

It is benign and the growth slow. 
Only dangerous by reason of strangu- 
lation or occlusion, as in digestive 
tract and weight in other cases. 

b. Rhabdoma or myoma striocellulari is 
a tumor of rare congenital form com- 
posed more or less of striated muscle 
fiber, together with a bulk of other 
tissue, which is generally sarcoma- 
tous. 

It is probably an inclusion from the 



TUMORS. 69 

embryonic muscle plates. 

It occurs chiefly in the kidney and tes- 
ticle. 

In structure its appearance is that of 
a spindle cell sarcoma, with more or 
less striped muscle fibers of an em- 
bryonic character. 

It is malignant in proportion to the 
sarcomatous element present. 

8. Neuroma is a tumor consisting of nerve 
tissue made up of principally medul- 
lated and non-medullated nerve fibers. 
Ganglion cells in the tumor are ex- 
tremely rare. 

Ordinarily growth of the perineurium or 
endoneurium are called neuromata, but 
these are purely fibromata. If with 
these there are any nerve fibers present 
the term fibroneuromata is used. 
The terms — 

a. True neuromata is used when the 
growth is strictly nervous, which is 
exceedingly rare. 

It is called — 

1. Myelinic when composed of med- 
ullated nerve fibers. 

2. Amyelinic when composed of 
non-medullated nerve fibers. 

b. False neuromata is used when the 
growth is of the nerve sheath, to- 
gether with the nerve fibers. 

The peripheral nerves are most fre- 
quently involved, but involvment 
may also be near their roots or the 
terminal fibers within the organs. 

The tumor is painful, but benign. 

9. Glioma is a tumor composed of neu- 
roglia. It is usually a solitary, round 
tumor, gradually merging into the sur- 
rounding nervous tissue, consisting of 
small spheroidal cells and the typical 
spider cells of neuro'glia. 

The protoplasm is scanty, while occa- 
sional fibers may render it moderately 
dense. 

The tumor is very vascular and hemor- 
rhage is frequent and followed by apo- 
plectic symptoms. Softening may oc- 
cur. 

Embryologically, it is an epithelial struc- 
ture, and therefore may be associated 
with sarcoma, though it is of slow 



70 PATHOLOGY. 

growth and essentially benign it causes 
great damage by its pressure on the 
nerve fibers or centers. 

It occurs in the brain and less fre- 
quently in the spinal cord. The cranial 
nerves are sometimes involved. 

Glioma of the Retina is primary, but may 
extend so as to involve the eyeball. It 
occurs most frequently in children, 
and family predisposition in some cases 
seems to play an important part. The 
growth is malignant in character. 

Glioma Ganglionare is a mixed tumor 
composed of neuroglia and nerve fibers, 
with large ganglionar nerve cells. 

It occurs as multiple nodular masses 
scattered through the brain or cord. 
The nerve roots and suprarenal cap- 
sules are sometimes the seat of these 
tumors. 

It may resemble the ordinary glioma. 
Its nature is the same as that of glioma. 

10. Haemangioma or Simple angioma is a 
tumor composed of new blood vessels. 
It is divided into — 

a. Capillary, Plexiform angioma or an- 
gioma teleangiectaticum is made up 
of arteries, veins and capillaries, 
which may have thicker walls than 
normal and be dilated or sacculated. 

It is most frequently found in the skin 
and forms the naevus, birth mark or 
port wine stain. 

It is usually conigenital, but may grow 
larger after birth. 

A condition where the vessels are much 
thickened and tortuous, forming the 
so-called "earth worm feel," bunches 
under the skin, is frequently seen in 
the varicosity of the legs, etc., and 
most frequently seen in hemorrhoids. 

b. Cavernous angioma shows a connec- 
tive tissue trabeculae, enclosing en- 
larged spaces lined with endothelium 
and filled with blood. 

They are tumor-like formations of a 
dark venous color, and are usually 
found in the skin or subcutaneous tis- 
sues. They are also found in the 
orbit, liver, spleen and kidney. 

It may be conigenital, but more fre- 
quently arises later in life. 





Fig-. 8. Myxoma, showing- stellate 
cells separated by a gelatinous (mucoid) 
intercellular material. 



fe^£ V *%0 'i; 

Fig. 9. Ch.ond.roma of the hyaline 
type. 












Fig-, 10. Cavernous angioma, (Warren.) 




Fig. 11. Adenoma of the mammary 
gland, with cystic enlargement of acini 
and abundant interglandular hyperplasia 
of connective tissue. 



TUMORS. 71 

It is a distinct tumor, which may show 
a distinct capsule. 

The plexiform angioma may be asso- 
ciated with lipoma, glioma and sar- 
coma. 

The angioma generally are essentially 
benign, and may continue throughout 
life, though hemorrhage, inflamma- 
tory or necrotic changes may take 
place. 

11. Lymphangioma is a tumor composed 
of dilated lymph vessels or lymph 
spaces, the latter more often involved. 
It is similar to the haemangioma and 

favors the same sites. 
Elephantiasis congenital mollis is a con- 
dition in which the subcutaneous tis- 
sues are edematous with cystic for- 
mations. 
Congenital cystic hygroma is a dilita- 

tion of the lymph spaces. 
Macroglossia is an enlargement of the 

tongue. 
Macrocheilia is an enlargement of the 

lips. 
Naevus lymphaticus is an enlargement 

of the skin. 
The above conditions are congenital en- 
largements dependent upon abnormal 
enlargement of the lymph spaces. 
Lymphangioma ^avernosum and caver- 
noma are the names sometimes given 
to these cases of dilated lymph spaces. 
It is a rare condition in which actual 
enlargement and varicosity of lymph 
vessels are found. It is, however, seen 
as a general process in elephantiasis. 
The acquired dilated lymphatics may 
attain a considerable size, and this 
rupture may lead to a dangerous 
lymphorrhea. The lymph may in this 
way be discharged externally, or it 
may be discharged into the various 
serous cavities. Rupture" along the 
urinary tract will occasion chyluria. 
It is a benign process generally. 
12. Lymphadenoma is a more or less ma- 
lignant new growth of the lymph glands 
or other lymphoid tissue, and has the 
structure of lymphatic tissue. Clinic- 
ally, it is called Hodgkins' Disease or 
Pseudoleukemia. 



72 PATHOLOGY. 

It can be considered as a form of sar- 
coma, or at least closely allied. It 
has been called lymphosarcoma, also 
malignant lymphoma and lymphoma. 

It presents itself as enlarged lymphatic 
glands of a single group or a number 
of groups in different parts of the 
body. 

A few or all of the glands in a group 
may be involved. The glands retain 
their shape, and as a rule do not ex- 
tend beyond their capsule. 

It may be soft or hard, according to 
the amount of connective tissue and 
the cellular infiltration and prolifera- 
tion present. 

The glands may be distinct or fused 
together. The tumor varies in size 
and shows up as knobby enlarge- 
ments under the skin. 

Microscopically, the glands in the 
earlier stages show a hyperplasia of 
lymphoid tissue, with a great number 
of small cells (lymphocytes). 

Later large cells with pale nuclei ap- 
pear. These are probably proliferated 
cells from the lymph sinuses. These 
may enlarge to become mononuclear 
or polynuclear giant cells, and at this 
time there is formed a reticular net- 
work, which increases till the gland 
becomes hard. 
Large areas of syncetial tissue (nu- 
cleated protoplasm) may be seen. 
The spleen may be involved, also the 
bone marrow, also the liver, kidneys, 
lungs, and the gastro-intestinal mu- 
cosa may be involved with new for- 
mations of the same character as that 
which takes place in the lymphoid 
tissue. 
13. Adenoma is a tumor which in struc- 
ture corresponds more or less to epithe- 
lial glands, but not in its function, as 
it is without proper secretion. 
It may arise from any active gland or 

from glandular "cell rests." 
In appearance it is moderately firm, 
usually single and circumscribed; 
sometimes it is surrounded by a 
fibrous capsule. 
Its epithelium is sometimes irregular, 
without a basement membrane and 



TUMORS. 73 

therefore abnormal, but it frequently 
conforms to glandular structure. 
There are two varieties — 

a. Tubular, in which the glandular sys- 
tem consists of tube formations lined 
with columnar epithelial cells. 

b. Racemose or alveolar, in which the 
acini are closely aggregated and cir- 
cular in outline, containing columnar, 
cubical or polyhedral cells. 

On account of its encapsulation in the 
breast and its superficial location 
in the rectum it is benign. In the 
stomach and when it affects the 
submucosa of the rectum it is very 
k malignant. It may undergo cystic 

change from the mucoid secretion 
(adenocystoma) or take on malig- 
nant characters by carcinomatous 
growth (adenocarcinoma). When 
there is a preponderance of fibrous 
tissue around the acini it is called 
adenofibroma. 

14. Papilloma is a benign tumor, which 
appears on the skin, such as warts, 
corns and horns, and on the mucous 
surfaces. 

There are two varieties — 

a. Hard papilloma, occurring on the 

skin. 

b. Soft papilloma, appearing on the 
mucous membrane. 

Papilloma is made up of a center or 
ground work of connective tissue 
containing blood vessels and cov- 
ered by epithelium. 

In the skin the growth appears as 
exaggerated papilla. A tendency to 
branching gives to it a cauliflower 
appearance; each branch contains 
a connective tissue framework and 
epithelial covering of stratified 
squamous cells, which show a tend- 
ency to horny change. 

In the mucous membrane the papil- 
lomata differ according to the situa- 
tion. 

Papilloma may greatly resemble an 
epithelioma, but can be readily dis- 
tinguished by the fact that papil- 
lomas growth is always superficial 
and always shows some connective 



74 PATHOLOGY. 

tissue stroma, while the epithelioma 
grows into the deep tissues. 
15. Carcinoma or cancer is a very malig- 
nant tumor, consisting of groups of 
epithelial cells arranged into solid 
blocks or columns separated by so- 
called alveoli of connective tissue, in 
which blood vessels alone are found. 
The epithelial proliferation shows a 
tendency to extend beyond its anat- 
omical limits. 

The structure of the cancer may be 
compared somewhat to a sponge, the 
sponge forming the alveoli, the can- 
cer cells filling up the holes. 

The histology of the cell, however, 

varies in different situations and in 

different forms. 
The epithelial cells vary in size from 

medium to large and have a large 

clear nucleus. 

The cell differs as to the structure in- 
volved. If of the skin the cells are 
large and usually of a squamous va- 
riety. If of the mucous membranes 
they are often cylindrical or col- 
umnar and with a tendency to the 
formation of cuboidal or polyhedral, 
which is generally present in cancer 
of the glandular organs. Secondary 
changes may change the appearance 
of the cells. The cancers of the skin 
may tend to arrange the epithelia in 
concentric whorls and tend to be- 
come glistening from horny trans- 
formation. 

The nucleus may be clear and quite 
structureless, or the nucleus may be 
distinct with a definite chromatin 
network. 

Karyokinetic figures may be abundant 
and frequently atypical. Degenera- 
tive changes may alter the nucleus 
as well as the body of the cell. The 
stroma is produced from the connec- 
tive tissue of the part at which the 
epithelium begins to grow abnormally, 
and is never found between the in- 
dividual cells, only around groups of 
them. The cells have no direct blood 
supply, but communicate freely with 
the lymphatics, through which meta- 
stasis, of the epithelium alone, oc- 
curs. The nearest lvmnh elands are 



TUMORS. 75 

therefore usually found enlarged and 
hardened. 

The metastatic epithelial cell attaches 
itself to a part and forces the connec- 
tive tissue to become its framework 
whether it be that of fibrous tissue, 
cartilage or bone. 

Macroscopically, carcinoma differ in 
appearance in different parts of the 
body. On the surface of the body 
they appear as nodular, flat eleva- 
tions. 

In the skin the nodules may be hard 
and smooth, or they may undergo 
ulceration. In the mucous membrane 
the growth is soft and polypoid 
ulceration may occur. 

In glandular organs the carcinoma are 
more or less nodular in form, or may 
be as irregular infiltrations. 

In consistency the tumor is described 
by the proportion of the cells to the 
connective tissue, as — 

Simple carcinoma, when the cells and 
the connective tissue are equal in 
amount, or nearly so. 

Hard, chronic or scirrhous, where there 
is a great preponderance of connec- 
tive tissue. 

Soft, medullary, acute or encephaloid, 
where there are large masses of cells 
with little stroma (brain-like in con- 
sistency). 

The scirrhous is of slow growth, but 
infiltrates the tissue widely. Meta- 
stasis and gland involvment is late. 

The situations in which carcinoma oc- 
cur are the mouth, in alimentary tract 
at the pylorus, ileocaecal valve 
larynx, gall bladder, uterus and some- 
times the other genito -urinary or- 
gans, liver and the lungs. 

Varieties of Carcinoma. 

a. Epithelioma is divided into — 
1. Squamous Epithelioma, which occurs 
in the skin or mucous membranes 
wherever stratified squamous epi- 
thelium exists normally. It spe- 
cially favors the junction of the 
skin and mucous membrane. The 
frequent seats are the lips, eso- 
phagus, larynx and cervix uteri. 
It is also seen in the anus and vulvi 



76 PATHOLOGY. 

and on the hands and feet of the 
aged. 

The lower cells of the Malpighian 
layer sends down cylinders of 
epidermis, which are cut off by 
connective tissue overgrowths and 
become "cell rests," which give rise 
to the concentric epithelial perles, 
epidermal globes, etc. 

Oblique sections of the normal epi- 
dermal prolongation or the glands 
should not be mistaken for the 
"cell rests." 

Epithelioma cells are large with 
prickle edge and frequent vacuola- 
tions of their substance. 

Metastasis is frequent, but it is not 
so malignant as the glandular car- 
cinoma. 
2. Cylindrical Epithelioma is made up 
of columnar or cylindrical epithe- 
lium. 

It is frequently seen in the mucous 
membranes of the gastro-intestinal 
tract and the uterus. The growth 
starts from the cells of the tubular 
glands or the surface. 

The structure is more or less of a 
tubular character, composed of a 
layer of epithelial cells or a num- 
ber of epithelial cell layers with 
the outer layer of columnar cells. 
The acini of the growth becomes 
filled with various shaped prolif- 
erated epithelial cells, or the 
tubular character of the acini may 
be lost. 

The carcinomata of the kidney, liver 
and mammary gland may be of the 
cylindrical form. This form re- 
sembles the glandular form, more 
than does the squamous, in its ma- 
lignancy. 

Rodent ulcer may be considered as a 
form of epithelioma of slow growth. 
It may begin as a wart or fissure 
of the skin and become a chronic 
ulcer, generally situated on the 
sides of the nose and around the 
orbit. It has a hard, overhanging 
edge. 

It shows no metastasis, nor are the 
glands involved. Prickle cells or 







Fig-. 12. Epithelioma of skin, showing: 
concentric arrangement and degeneration 
of cells. 




Fig. 13. Careinoma of uterus. 




Figr. 14. Scirrhous carcinoma. 




Medullary carcinoma of 



TUMORS. 77 

perles are not found. 

b. Glandular carcinoma resembles race- 

mose glands, being made up of 
alveoli containing epithelial cells in 
several layers, which fill the lumen, 
and a connective tissue stroma. 

They may be divided into three forms — 

1. Simple, made up of epithelium and 

stroma, resembling more or less the 
structure of normal glands. 

2. Medullary or soft is made up of an 

excessive amount of epithelium in 
the form of solid plugs or columns 
of epithelial cells. 

3. Scirrhous is where there is a mix- 

ture of acini and epithelial cells, 
but with an excess of fibrous tissue, 
which renders it hard. 
The glandular variety of carcinoma 
is more or less nodular or infil- 
trating and glistening white in 
color. On section a milky fluid ex- 
udes, which is made up of an al- 
buminous fluid, degenerated cells 
and oil droplets. 

It is found in the pylorus, other mu- 
cous surfaces, mammary gland, 
pancreas, kidneys, ovaries and tes- 
ticles. 

Metastasis occurs. 

c. Colloid cancers are seen in the stom- 

ach and intestinal tract, mammary 
gland and ovaries. It is jelly-like 
and of a transparent, glistening ap- 
pearance. 

Microscopically, there is a mucoid de- 
generation of the epithelial cells and 
the connective tissue. In some cases 
the epithelium alone is involved. 

Direct extension is a frequent method 
of spreading. The entire abdominal 
cavity may become filled with the 
material. 
16. Sarcoma is a malignant tumor made 
up of connective tissue cells with 
little inter-cellular substance. It is 
more or less rounded in form and 
often encapsulated. It may. however, 
be irregular, infiltrating and there- 
fore without a capsule. 

In consistency it is flesh-like, hard or 
soft, depending upon the proportion 
of cells and inter-cellular substance, 



78 PATHOLOGY. 

or according to the amount of asso- 
ciation with fibroma, chondroma, 
myxoma, etc., and with adenoma. 

It is white or gray and on section a 
whiteish, liquid exudes. 

Dilated blood vessels may give it a 
hemorrhagic appearance or actual 
hemorrhage may take place with for- 
mation of cysts, bloody or serous. 
Necrosis, mucoid change or liquefac- 
tion necrosis may render the sar- 
coma soft and cystic. 

Secondary sarcomata are nodular in 
character and usually have a cap- 
sule. White or pinkish in color, firm, 
but with a tendency to central 
necrosis or softening. In some cases 
where the body is studded with white 
spots, like those of miliary tuber- 
culosis, the condition is called sar- 
comatosis. 

In structure the main type of cells are 
round, cylindrical, spindle shaped or 
polymorphous. The nucleus is vesic- 
ular, though sometimes granular, and 
occupies a large proportion of the 
cell. If the growth is rapid, karyo- 
kinetic figures may be abundant. 

The arrangement of cells is very ir- 
regular. The inter-cellular substance 
is homogenous with a few fibers in 
the spindle variety, but few if any 
in the other forms. 

The distinctive feature of the growth 
is the presence of connective tissue 
and blood vessels between the indi- 
vidual cells which have no direct con- 
nection with the lymphatics. Meta- 
stasis is therefore by the blood ves- 
sels, hence appears earlier than in 
carcinoma. 

Sarcoma springs from pre-existing con- 
nective tissue, such as the subcutane- 
ous, intermuscular, periosteal, tendi- 
nous, bone, cartilage, fat, lymphatic 
glands, submucous and serous sur- 
faces. 

They are also found in the kidney, 
liver, spleen, thyroid gland and 
testis. 
Varieties of Sarcoma. 

a. Round-celled sarcoma is made up 



TUMORS. 79 

of small or large round cells with 
little intercellular substance. 

It springs from any form of connec- 
tive tissue, but frequently affects 
the skin (moles and warts) and 
bones, and is of a soft consistency. 

The small cell variety is softer than 
the larger. Both are very ma- 
lignant; the smaller is perhaps the 
most malignant of all varieties. 

1. Lympho sarcoma is a variety of 

the round cell sarcoma. It re- 
sembles the structure of a 
lymphatic gland. It is character- 
ized by a reticular stroma formed 
by stellate cells, which are united 
by their prolongations. 
It occurs in the lymphatic glands 
and lymphadenoid tissues of the 
mucous membranes. The thymus 
gland and other organs may be 
affected. 

Lymphosarcoma, unlike lymphade- 
noma, shows a tendency to ex- 
tend beyond the normal limita- 
tions of the gland or its other 
structure. 

Chloroma is a round cell sarcoma, 
which occurs in the periosteum 
of the bones of the head and 
secondarily in other parts of the 
body. On section it is first green 
in color, then by exposure to the 
air it is changed to gray. 

Clinically, it is associated with 
symptoms of leukemia or pseu- 
doleukemia. 

2. Alveolar sarcoma is a variety of 

the round celled sarcoma, though 
there is also spindle cells pres- 
ent. 

Its characteristic features is the 
acinus structure, composed largely 
of spindle-shaped cells with some 
fibrillar, intercellular substance, 
filled with large round cells, hav- 
ing a more or less epitheloid ap- 
pearance. 

It is frequent in the skin, spring- 
ing from warts and moles. It oc- 
curs also in lymph glands and 
serous membranes, etc. 



80 PATHOLOGY. 

b. Spindle cell sarcoma is made up of 

large or small spindle-shaped cells, 
with slender or sometimes branched 
ends. 

The cells may be angular or stellate. 
The cells may run in parallel col- 
umns or they may run in different 
directions. The spindle celled sar- 
coma is of a denser consistency 
than the round celled sarcoma, 
and usually more grayish or flesh- 
colored. It is often associated 
with fibromata, with which it may 
be confused. 

It is found in the denser connective 
tissue of periosteum, tendons and 
fascia. 

It is less malignant than the round 
variety and shows no tendency to 
metasasis, but recurs after re- 
moval. 

c. Angiosarcoma or Perithelioma is a 

sarcoma which arises from the 
adventitia of blood vessels. It re- 
sembles carcinoma. 

The tumor is generally quite vascu- 
lar and is seen in the serous mem- 
branes and skin, and especially in 
the salivary glands. Its character- 
istic feature is the round-cell 
masses surrounding the blood ves- 
sels. 

Plexiform angiosarcoma is the name 
given to it when each vessel of a 
vascular network is surrounded by 
a coat of sarcoma cells. 

Alveolar angiosarcoma is the name 
given to it when the vascular net- 
work encloses the sarcoma cells in 
such a way as to give rise to an 
alveolar form. These forms are 
found in the sarcomata of warts 
and moles and are prone to mela- 
notic change. 

The endothelium of the blood vessels 
is sometimes the origin of vascular 
sarcoma and is a rare variety of 
endothelioma. 

They are liable to degenerations, 
such as myxomatous and hyaline. 

Angiosarcoma is somewhat benign. 
Metastasis as a rule is rare, but 




Fig-. 16. Small round-celled sarcoma; 
in the center is seen a blood vessel with 
its wall of endothelium. 




Fig-. 17. Lymphosarcoma of nasal mu- 
cous membrane; a, on left side a blood 
vessel, on right side reticulum; b, cells 
of reticulum; c, sarcoma cells. (Zieg*- 
ler.) 




Fig-. 18. Angiosarcoma with myxoma- 
tous degeneration (cylindroma) ; the fig- 
ure represents one of the blood vessels 
with the sarcomatous cells springing" 
from its walls and outside of these 
myxomatous tissue. 







Fig-. 19. Cylindroma, showing a num- 
ber of blood vessels whose walls have 
become converted into hyaline material. 



TUMORS. 81 

the alveolar and the melanotic 
variety are very malignant. 

d. Cylindroma is a variety of the peri- 

thelioma and receives its name 
from the cylinders of sarcomatous 
cells growing around the blood 
vessels. 

Sarcomatous cylindromata, may be 

simple sarcoma, which has under- 
gone hyaline or myxomatous 
degeneration, or the two combined 
more or less, but nearly always it 
is the angiosarcomata which pre- 
sents the condition. 

The sarcoma cells surrounding the 
blood vessels are converted into 
hyalomyxomatous tissue, resulting 
in branching columns of the ma- 
terial which traverses the sar- 
coma. 

Angiosarcomata myxomatodes is the 
term used when the walls of the 
blood vessels themselves are the 
seat of hyaline change, the 
sarcoma cells are pushed aside. 

Cylindroma occur in the salivary 
glands, brain, lachrymal glands and 
sometimes in the subcutaneous tis- 
sue. 

It is more or less benign. 

e. Endothelioma begins in the endo- 

thelium of blood or lymph vessels 
and spaces. It occurs in the se- 
rous membranes, as the pleura, 
peritoneum and meninges, but it 
may be found in the skin, walls 
of blood vessels, periosteum, bone 
marrow, lymphatic glands, gums, 
ovary, testicle, liver and salivary 
glands. 
It has, by its growth along the ves- 
sels, a more or less tubular or 
acinus-like aggregation of endo- 
thelial cells. Frequently it orig- 
inates from the endothelium sur- 
rounding the blood vessels. The 
endothelium of the perivascular 
lymph spaces proliferate and form 
a growth around the blood ves- 
sels, which is really an angiosar- 
coma or perithelioma, and by its 
mucoid or hyaline degeneration 
cylindroma may take its origin. 



82 PATHOLOGY. 

f. Melanosarcoma, Melanotic sarcoma, 

Melanoma, Chromatophoroma or 
Pigmented sarcoma is a very ma- 
lignant tumor, consisting of round 
or spindle cells, or both, in which 
there is abundant melanin (chro- 
matophores) and stroma. 

The pigment gives to it a dark 
color. It is found in the skin, es- 
pecially in pigmented moles or 
warts and in the choroid of the 
eye and the pia mater. 

The tumor is extremely malignant, 
grows very rapidly and shows 
early and wide metastasis, espe- 
cially the lymphatic glands and 
later the liver. 

This tumor is a definite growth and 
is not merely a pigmented sar- 
coma. 

g. Giant-celled sarcoma, Myeloid sar- 

coma, Osteosarcoma is made up of 
large round or spindle cells inter- 
mingled with large multinuelear 
cells which resemble the myelo- 
plaques of bone. 

The tumor generally grows in con- 
nection with bone, does not show 
metastasis and as a rule does not 
recur after removal. 

The giant cells may be said to be 
due to irritation of the spicules of 
bone or the deposit of blood pig- 
ment, and are therefore mere ac- 
cidents in a round or spindle cell 
sarcoma. 
The maxillary bone is most fre- 
quently involved. An epuiis grow- 
ing from the dental alveoli is of 
this nature. 
17. Cysts are pathologic formations, con- 
sisting of a more or less definite 
wall, enclosing a liquid or semi- 
liquid substance, which differs in 
character from the surrounding parts. 
Some cysts are true tumors; others 
are quite different in nature. Some 
cysts do not have a definite capsule, 
hence we distinguish — 
St. True cysts, which are enclosed by a 
capsule and is lined by epithelium 
GT endothelium. 



TUMORS. 83 

b. Cystoids (cyst-like formations), 
which are merely a circumscribed 
collection of softened material. 

Cysts may be classified as— 

1. Retention cysts are formed when 

the outlet of any secreting struc- 
ture is obstructed, as when the 
duct of a sebaceous gland of the 
skin is closed, causing the so- 
called sebaceous cyst or wen. 
Ranule is the term used when 
the cyst is due to the closure 
of the salivary or small mucous 
glands or ducts under the 
tongue. 
Cysts are also formed by the clos- 
ure of the uriniferous tubules, 
tubules of ovary or in par- 
ovarium, in acini and ducts of 
the mammae, pancreas and other 
glands. 

2. Softening cysts are due to degen- 

erative softening of the normal 
or pathologic tissues. 

It may be the result of hemor- 
rhage, the blood clot is inspis- 
sated and followed by exudation 
of serum in the area. 

This form is common in all the 
different kinds of tumors. 

Softening cysts may also be due 
to foreign bodies. The tissues 
having been injured by the same, 
they undergo necrosis with the 
formation of a capsule by con- 
nective tissue reaction. Fre- 
quently seen as a result of para- 
sitic invasion. 

3. Proliferation Cysts. This forma- 

tion is very much like true 
tumors. They are sometimes 
called epithelial cysts. They oc- 
cur in glandular organs, such as 
the ovary and mammary gland, 
or they may appear in any gland. 

They may represent an adenoma- 
tous or carcinomatous new 
growth. 

They result from obstruction to 
the excretory ducts and the irri- 
tation of the retained secretion. 
Congenital abnormalities may 



84 PATHOLOGY. 

also play a part in their forma- 
tion. 
It may be in the form of a single 
cyst, or it may be multiple, or 
the large cyst may be divided by 
compartments into many and 
filled with a serous, gelatinous 
or hemorrhagic fluid. 

Secondary degenerations may oc- 
cur. They may be benign, but 
often there is a tendency to ma- 
lignancy, frequently undergoing 
a carcinomatous change, which 
spreads or becomes metastatic. 

II. TERATOMATA is a tumor of a pe- 
culiar, mixed character, representing 
the products of growth of one indi- 
vidual within the tissue of another in- 
dividual of the same species. It is 
probably due to some congenital mis- 
development. It may be — 

Endogenous, in which superficial tis- 
sues are retained in the internal 
parts. 

Ectogenous, in which there is a sep- 
arate foetal deposition, as the origin 
of the tumor. This is seen when 
there is a separate and well-devel- 
oped foetus within the developed or- 
ganism (a foetus in foetu). 

1. Dermoids or Dermoid cysts are cystic 

formations which are found in the 
skin in the regions of the neck and 
sacrum and in the ovary, less often 
in the brain, testis, orbit and lungs. 

They are filled with a semi-fluid, 
cheesy mass, consisting of epithelial 
cells, fatty matter, hair, teeth, mus- 
cle, bone, and glandular structure 
also occur. 

A tumor called cholesteotoma of a 
glistening, whitish nature and com- 
posed of concentric layers of cells re- 
sembling epithelium, with occasional 
crystals of cholesterin, is sometimes 
found in the membranes and sub- 
stance of the brain, is classed by 
Ziegler as teratoid growths. 

Similar growths are found in the kid- 
neys, testicles, parotid gland, ovary 
and middle or external ear. 

2. Syncytioma malignum or Deciduoma 

malignum or Sarcoma Deciduocellu- 



BACTERIA. 85 

la re is a very malignant tumor of the 
decidua. 

It of course occurs during pregnancy 
and originates at the site of the 
decidua serotina, but rapidly spreads 
to the uterus and then by metastasis 
through the blood vessels to the ex- 
ternal genitalia, frequently the lungs 
and less often the liver, spleen and 
other organs. 

The nature of the tumor is still un- 
determined. It is probably a foetal 
structure composed of large and 
small cells. The larger cells growing 
from the syncytium and the smaller 
cells from the outer epiblastic cov- 
ering of the chorionic villi (Langh- 
an's cells). 

It is therefore carcinomatous, though 
its metastasis suggests sarcoma. It 
is very vascular and therefore sub- 
ject to hemorrhage. 

BACTERIA AND DISEASES DUE TO 
BACTERIA. 

FUNCTIONS AND PRODUCTS OF 
BACTERIA (Vital Actions). 

The vital actions of bacteria are de- 
structive ones, splitting up higher 
nitrogenous and non-nitrogenous 
compounds into simpler substances. 
Sometimes such changes are destruc- 
tive to the bacteria themselves, as 
when lactic and butyric acids are 
formed in the media. 

As producers of disease bacteria cause 
various pathologic conditions, pro- 
ducing diseases known as infectious 
diseases, and the germs are called 
pathogenic bacteria. 

The germs which do not cause any 
pathological conditions are called 
non-pathogenic bacteria. 
The substances found in media of bac- 
terial growth are — 
1. Proteins, which are components of the 
bacterial cell proper and may cause 
suppuration (Pyogenic), fever ( Pyro- 
gen ic) and inflammatory processes 
(Phlogenic). 

Some examples of this is mallein (de- 
rived from the bacillus of glanders), 
and tuberculine (derived from the 



86 PATHOLOGY. 

bacillus of tuberculosis). 
These when injected into subjects sick 
with the disease are pyrogenic, but 
in healthy subjects they have very 
little or no effect. 

2. Ferments, secretions of the cell, pos- 
sess the power of breaking up the 
more highly organized nitrogenous and 
non-nitrogenous compounds into sim- 
ple and more diffusible substances. 
The action of ferments upon non- 
nitrogenous compounds is called fer- 
mentation. 
The action of ferments upon non- 
nitrogenous compounds is called pu- 
trif action, which often produces odor- 
ous gases and ptomains (complex al- 
kaloids resembling those found in 
plants). 

The principal bacterial ferments are— 
Proteolytic, transforming albumin into 
more soluble substances, gelatin 
liquefaction is an example; diastatic 
transforms starches into sugar; in- 
verting changes a sugar that does 
not undergo fermentation into one 
that does; emulsifying formed by a 
few microbes, e. g., micrococcus pyo- 
genes tenuis; coagulating coagulates 
milk; others produce both a coagula- 
tion and a dissolving ferment 
(casease), which dissolves the coagu- 
lation; hydrolytic breaks up urea into 
ammonium carbonate and hippuric 
acid into glycocol and benzoic acid; 
fat splitting splits fats into glycerin 
and fatty acids; oxidizing reduces the 
nitrates of the soil into ammonia, 
etc.; nitrifying changes albuminoids 
into skatol, indol, leucin, and these 
into ammonia, ammonia into nitrites, 
and nitritis into nitrates. 

3. Substances that are the result of the 
action of bacteria upon the medium 
of growth — 
a. Toxins are poisonous substances 
akin to the venom of serpents and 
other animals, and to certain pois- 
onous principles of plants. It has 
been estimated that 1-1000 gm. of 
tetanus toxin will kill a horse 
weighing 1,200 pounds. 
They were first called ptomains or 



BACTERIA. 87 

cadaveric alkaloids, but this term 
is now applied to poisons which 
form in decomposing meat, cheese, 
etc., as a result of chemical change 
caused by bacteria. They have 
.also been termed toxalbumins, as 
' they give all the reactions of albu- 
mins. 

It is probable, however, that a tox- 
albumin is but a combination of 
the toxin and the substances de- 
rived from the medium of growth. 

Toxines may be divided into — 

1. Those which are within the body 
of the bacteria and are set free 
by the disintegration of the or- 
ganism. Pathogenic bacteria 
comprise most of this group. 
Anti-bacterial sera is used to 
combat this type. 

2. Those in which the toxines are 
excreted by the bacteria and are 
found in the surrounding media. 
Anti-toxic sera is used to com- 
bat this type. 

b. Pigments. Bacteria have the prop- 
erty of forming pigments in them- 
selves (chromophoric, or they form 
a chromogenic body which when 
free gives rise to color (chromo- 
paric). 

C. Photogenesis, phenomenon of phos- 
phorescence, e. g., condition seen 
in decaying fish, etc. 

d. Fluorescence. A play of colors is 

found in some bacterial cultures. 

e. Odors are produced by some germs, 

some pleasant and others foul. 

f. Gas is formed by anaerobic bacteria, 

especially noxious and odorless. 
Effect of Bacteria, generally known as 
Infections. 
When bacteria have gained an entrance 
into the animal body they may pro- 
duce effects in two ways— 
1. Local Effects. The local effects of bac- 
teria are of two kinds — 
a. Mechanical. By their mere presence 
in the tissues bacteria may cause 
tissue changes of two kinds — 
t. Proliferation, due to irritation. 
2. Thrombosis (by rapid multiplica- 
tion) and its consequent conditions, 



88 PATHOLOGY, 

b. Toxic. The local toxic effects of bac- 
teria are due to the action of their 
toxins upon the cells with which 
they are in direct contact, and may 
be,— 

1. Proliferation. • 

2. Cell degeneration, and 

3. Necrobiosis. 

2. General Effects (Intoxications). 

The general effects of bacteria upon 
the body are due entirely to the cir- 
culation of their toxines in the blood. 
This may occur in two ways, viz., 
from — 

a. Primary focus (point of entrance). 
Bacteria may remain at the point of 

entrance and elaborate toxins 
which are absorbed and circulated 
by the blood, causing disease, e. g., 
tetanus, diphtheria and the sapre- 
mia due to pyogenic organisms. 

b. Secondary foci. 

Bacteria may also circulate in the 
body fluids and find lodgment in 
any of the organs, causing both 
local tissue changes and general in- 
toxication, e. g., Bacillus of Eberth 
(typhoid fever), Pneumococcus of 
Frankel (pneumonia), Diplococcus 
intracellulars of Weichselbaum 
(cerebro-spinal fever), Streptococus 
(septicemia and pyemia). 
Conditions Necessary to Infection are — 

1. The micro-organism must be patho- 
genic. It must be a parasite. 

2. Toxins elaborated by the micro-organ- 
ism must be present in sufficient 
amount. 

3. Animal infected must be susceptible. 

SUSCEPTIBILITY. 
Susceptibility varies. It may be — 

1. Natural, to a certain race. 

2. Aquired, to those conditions being 

present which lower vitality. 

3. Inherited, by reason of inherited 
tendency. 

IMMUNITY. 
-.- Immunity denotes that condition of 
■ an organism which enables it to 

resist an- attack of the - particular 
bacteria and their- toxic secretions 
against - which they -are- said to be 
immune,,. •;,■••• ...... 



IMMUNITY. 89 

The varieties of immunity are 

1. Natural, as an inheritance from im- 

mune ancestors. 

a. Absolute immunity is rare. 

b. Relative immunity is common. It 

may be individual or racial, e. g., 
dogs and Algerian sheep are resist- 
ent to anthrax. 
Lower animals are immune from cer- 
tain diseases common to man, e. g., 
sphilis. 

2. Acquired. 

a. Active immunity. 

1. Naturally acquired by a previous 

infection. 

2. Artificially acquired by — 

a. Inoculations with weakened, at- 

tenuated cultures of bacteria, 
e. g., vaccins of variola and 
anthrax. 

The attenuation is produced by 
successive artificial cultivations. 

Virulence is lessened by passing 
cultures through animals less 
susceptible or immune. 

b. Inoculation of small doses of 

very virulent micro-organisms. 
Successive inoculations with 
gradually increased doses of the 
virus creates an immunity suf- 
ficient to resist 10 times the 
toxic dose. 

c. Injecting gradually increased 

doses of the sterilized or fil- 
tered products of bacteria. 
Cultures are sterilized by heat 
or filtered through germ filters. 
The sterilized cultures or the fil- 
trate still contain the toxins. 

b. Passive immunity is acquired by the 
injection of the serum of animals 
that have been rendered immune by 
the artificial methods. 

THEORIES OF IMMUNITY. 

The theories most acceptable at the 
present time are modifications of 
MetchnikofTs Phagocytic and Ehr- 
lich's "side chain." 
MetchnikofTs Phagocytic op Cellular 
Theory. 
The term "phagocyte" is given to any 
cell capable of incorporating bacteria 



90 PATHOLOGY. 

and of destroying them by a process 
of digestion. 

Phagocytic cells comprise — 

1. Microphages, polymorphonuclear leu- 

cocytes. 

2. Macrophages are all other leuco- 

cytes, endothelial cells and connec- 
tive tissue corpuscles, having pha- 
gocytic power. 

When animals are subjected to an 
irritant ' phagocytosis occurs. The 
leucocytes are attracted by chemo- 
taxis to the zone of irritation and 
envelop the irritating substance. 

The organisms that escape from one 
cell are seized by others, but if 
their multiplication is excessive 
they overpower the phagocytic leu- 
cocytes and invade the blood 
serum. The blood serum and the 
body fluids are likewise bacteri- 
cidal, due to the disintegration of 
phagocytes — phagoiysis; the prop- 
erties of these cells being imparted 
to the serum. This property is due 
to two constituents of the plasma. 
The one (the specific immune 
body) circulates in the plasma and 
resists a temperature of 100 de- 
drees C. The other, or "cytase" 
(digestive ferment), derived from 
the disintegrated phagocytes, cor- 
responds to Buehner's "alexins" 
and Ehrlich's "lysins." It is de- 
stroyed at 60 degrees C. 

Ehrlich's "side chain" theory derives its 
name from its analogy to what hap- 
pens in the Benzol ring when its re- 
placeable hydrogen atoms are substi- 
tuted by "side chains." The theory 
itself is based upon the mechanism 
of cell nutrition in its relation to the 
mode of production of specific anti- 
toxines. Each cell contains an active 
central nucleus and outer groups of 
molecules or "side chains" (recep- 
tors). These outer groups make up 
the main feature of the scheme, 
since the receptors receive the nu- 
trient molecules (haptophores) by 
which the cellexists. The receptors 
have an affinity for the haptophores, 
but do not combine with these only. 



OPOSONINS. 91 

The cells may, by means of the re- 
ceptors, take up in addition any num- 
ber of isomeric non-nutritious bodies, 
and if any of these happen to be 
toxic (toxophore) and sufficiently ac- 
tive in quality and quantity, the 
cell's function is inhibited or de- 
stroyed. 

Intoxications being due to a toxin, the 
toxophore attaches itself to the re- 
ceptor and reacts actively upon the 
cell proper. 

The receptor being destroyed, the cell 
reproduces a greater number of new 
ones than are required by the cell 
itself, therefore they accumulate in 
the blood and lymph. The surplus 
receptors (antitoxins) preserve their 
affinity for their specific toxophores 
and hold the toxin in captivity, as it 
were, before it can reach the cell 
proper, thus immunizing the cell 
against the poison. The destruction, 
by the blood serum, of the bacteria 
(bacteriloysis), worn-out blood cells 
(haemolysis), muscle cells (myolysis), 
etc., is probably brought about by a 
destructive solvent element called 
the "compliment" (lysins, alexins or 
cytase) and an "immune body" (An- 
boceptor), which attaches itself to 
the cells or the bacteria to be dis- 
solved, and acts as a link between 
them and the compliment. It is in 
this way that the compliment, which 
has no affinity for the cellular ele- 
ments, is brought into contact with 
the cells to be dissolved. 
Opsonic Theory. 

Wright and others have demonstrated 
certain thermolabile bodies, the ac- 
tive products of the tissues and 
serum under the stimulation of the 
toxin, which, acting upon bacteria, 
sensitize them for phagocytosis. 
These substances have been called 
opsonins. ■ 

They have a haptophore group which 
attaches themselves to the bacteria 
and an opsoniferous group which re- 
sembles the complements. Chemic- 
ally, they are unstable, as they un- 
dergo changes at 60 degrees C. or by 
the action of light. 



92 PATHOLOGY. 

OTHER REACTIONS OF IMMUNITY. 

Specific precipitins are substances which 
are precipitated when immune bodies 
are brought into contact with the 
specific body of whose stimulation it 
is formed. In other words, the blood 
serum of animals immune against 
certain bacteria or their albumins 
will give a precipitate when added 
to the cultures of these organisms or 
their albumins. The nature of this is 
not understood. 

Agglutinins. If certain bacterial cultures 
be added to the blood serum of an 
animal whose illness is due to that 
particular organism the bacteria will 
become clumped in motionless masses. 
This condition is taken advantage of 
by Widal for diagnostic purposes — 
typhoid fever, etc. 

DISEASES DUE TO BACTERIA. IN- 
FECTIOUS DISEASES. 

An infection is the invasion of the 
body by a disease producing micro- 
organism. The time when the germ 
enters the body is not always known 
to the patient, and some time usually 
elapses between the time of actual 
entrance and the appearance of the 
resulting symptoms. This time is 
called the period of incubation. 

There is, at this time, no great dis- 
tinction between the terms infection 
and contagion unless it is that in 
contagion it is used to denote infec- 
tion by personal contact. 

SUPPURATIVE DISEASES. 

1. STAPHYLOCOCCUS GROUP may be 

divided into — 

a. Staphylococcus pyogenus aureus is 

found in lesions such as furuncles, 
abscesses, carbuncles and ulcera- 
tions of the skin or mucous mem- 
branes. It is frequently seen in 
suppurative inflammations, such as 
malignant endocarditis, osteomy- 
litis, appendiceal abscesses, etc. 
It is generally found in focal lesions. 
Other organisms may also be as- 
sociated in these lesions. 

b. Staphylococcus pyogenes albus is 

far less virulent than the aureus 



BACTERIA. 93 

and is frequently found as a harm- 
less parasite of the skin. Asso- 
ciated with other micro-organisms 
it occurs generally in abscesses and 
suppurative diseases. 

c. Staphylococcus pyogenes citreus is 

not very common nor virulent. 

2. STREPTOCOCCUS GROUP. Under 

the streptococcic group are included 
various bacteria that resemble each 
other very closely. 

a. Streptococcus pyogenes is found dis- 

tributed much the same as is the 
staphylococci, but not generally in 
the healthy body. 

It is found upon the mucous mem- 
branes or in the various secretions 
or excretions of the body, and oc- 
curs occasionally in focal lesions. 

It may occur in generalized septo- 
pyemia, infectious endometritis and 
sometimes in ulcerative endocar- 
ditis. 

It may occur in persons with a previ- 
ous good health or in the course of 
infectious diseases, such as scar- 
latina, measles and la grippe; also 
in sore throats resembling diph- 
theria (pseudodiphtheria). It is 
always found in all cases of ery- 
sipelas. 

b. Streptococcus intracellulars menin- 

gitidis, also called meningococcus 
or diplococcus meningitidis, is found 
in meningeal pus, nasal mucus, 
sputum and urine of those sick 
with epidemic cerebro-spinal men- 
ingitis. 
Other micro-organisms associated in 
meningitis are the pneumococcus, 
streptococcus and staphylococcus 
pyogenes, typhoid and colon 
bacilli, influenza bacillus, etc. 

3. GONOCOCCUS OF NEISSER is a 

diplococcus which occurs in the pus. 
epithelial cells and deeper structures 
of the urethra in gonorrhoea, of 
which it is the specific cause. Gon- 
orrhoea is generally a local disease, 
but it may extend to the neighbor- 
ing structures, as the testis, uterus 
and tubes. It may also, secondarily, 
cause arthritis, peritonitis, endocar- 



94 PATHOLOGY. 

ditis, conjunctivitis, etc.; the latter 
(gonorrhoeal opthalmia) is a^ very 
grave affection. It may also give rise 
to peripheral abscesses, suppurative 
adenitis, etc. 

4. DIPLOCOCCUS PNEUMONIA, pneu- 

mococcus, micrococcus lanceolatus, 
streptococcus pneumania seu lance- 
olatus. This micro-organism is of 
lanceolate shape, and in the sputum, 
lungs and in the blood it is com- 
monly found in pairs, with its broad 
ends adjacent and the pointed ends 
out. 

The specific character of this organism 
has not been determined definitely 
according to Koch's rules, though it 
is considered the usual cause of 
croupous pneumonia. 

The germ first produces local lesions 
within the lung, then systemic infec- 
tion and general intoxication when 
the organism gains access to the 
blood. It may now also produce sec- 
ondary lesions in other organs. The 
germ has been found in other condi- 
tions, such as meningitis, pleurisy, 
inflammation of other serous sur- 
faces, abscesses, otitis media and 
arthritis. 

Irregular forms of lobar pneumonia 
may be caused by the streptococcus 
or the staphylococcus, influenza 
bacillus, typhoid bacillus and Fried- 
lander's bacillus of pneumonia. 

5. BACILLUS PNEUMONIA OF FRIED- 

LANDER occurs as a distinct bacil- 
lus, usually in pairs and surrounded 
by a capsule. It was at one time re- 
garded as the cause of croupous pneu- 
monia. 

It may sometimes be the cause of the 
catarrhal or lobular form, or the ir- 
regular forms of pneumonia of the 
ordinary croupous pneumonia. It. 
however, probably occurs as a mixed 
infection. 

When a pneumonia is due primarily to 
this bacillus it is very virulent, caus- 
ing a peculiar visid exudate in the 
lung. 

Other organisms found in broncho 
pneumonia are the streptococcus 



BACTERIA. 95 

pyogenes, occasionally the influenza, 
coli communis, typhoid, glanders and 
the plague bacillus. 

6. BACILLUS RHINOSCLEROMATIS is 

allied to Friedlander's bacillus and 
causes a condition called Rhino- 
scleroma, which presents itself as 
nodular thickenings of the skin of 
the nose and lip, and sometimes 
spreading to neighboring parts, as 
the mucous membranes of the mouth, 
pharynx or larynx. The mucous 
membranes are prone to ulcerate, the 
skin rarely. 

The cells involved may suffer hyaline 
degeneration. 

7. BACILLUS OF DIPHTHERIA (Klebs- 

Loeffler Bacillus) is the specific cause 
of diphtheria, which is primarily a 
local disease of the tonsils, pharynx, 
larynx and mucous membranes or 
skin, and produces a pseudomem- 
brane, which is made up of a fibrinous 
exudate in which are massed epithe- 
lial cells, other tissue elements and 
infiltrating leucocytes. The affected 
membranes undergo coagulation ne- 
crosis or granular degeneration. The 
action of the toxins may produce in- 
ternal or viseral lesions during its 
course or during convalescence. De- 
generation of the nerves and muscles 
with later paralysis, which may be 
temporary or total, together with ne- 
crotic lesions in the liver or other 
organs, myocarditis or myocardial 
degenerations, renal degenerations 
and nephritis are all complications 
met with. 

The organisms are found locally— that 
is, in the pseudomembranes in enor- 
mous numbers, but only exception- 
ally are they found in the blood or 
in the internal organs. 

A non-pathogenic diphtheria bacillus 
is found in the pharynx of healthy 
people as well as in other parts of 
the body. It is also found in the 
various forms of rhinitis, conjunc- 
tivitis and non-diphtheitic angina. 

The germ differs from the virulent 
diphtheria bacillus, in that it is 
harmless and also in its morphology. 



96 PATHOLOGY. 

It is called the pseudodiphtheria 
bacillus, and its exact relation to the 
Klebs-Loffler bacillus is still unset- 
tled. 
Other organisms, such as the strepto- 
cocci and staphylococci and the pneu- 
mococci, may be associated with the 
bacillus of diphtheria and take a 
prominent part in the local or gen- 
eral pathologic process of the dis- 
ease. 
8. BACILLUS TYPHOSUS, B. TYPHI 
ABDOMINALIS, is the specific cause 
of typhoid fever (enterica or enteric 
fever). It is a very motile bacillus 
containing 18 to 20 peripheral flagella. 
It is short, somewhat plump and has 
rounded ends. It occurs both within 
and without the human body. Within 
the body it occurs in lesions of the 
intestine and intestinal contents and 
is often present in the spleen, liver 
and kidneys. It is regularily found 
in the blood and is almost present in 
the gall bladder. 
It also occurs in the lungs, parotid 
gland and other organs and post 
typhoidal abscesses. 

The brunt of the attack usually falls 
upon the solitary and agminated 
glands of the intestines which show 
every change from inflammation and 
superficial ulceration to a deep 
necrosis with perforation and 
peritonitis. 

The ulceration is generally located 
at the lower end of the ilium but 
may be as far up as the jejunum 
and as low down as the rectum. 

The necrosed condition frequently 
causes hemorrhage which is often 
fatal. 

The typhoid ulcer is usually oblong 
with its long axis parallel with that 
of the bowel in contradistinction to 
the tuberculous (annular) ulcer which 
is transverse. 

A similar affection is found in the 
mesenteric glands and the spleen 
which is nearly always more or less 
enlarged. 

The inflammatory condition extends to 
the surrounding mucous membranes 



BACTERIA. 97 

causing catarrhal change (diarrhoea) 
and the toxin produced by the bacillus 
may cause focal necroses of the 
vicera, infarction and thrombosis with 
the conditions which follows such as 
gangrene of the lung and bowel and 
embolism of different organs. 

The infection may be followed by 
pneumonia, myocarditis, inflamed kid- 
neys and ovaries, and suppurative in- 
flammation of most any organ, 
periosteum of bone or the connective 
tissues. 

Protective vaccination (Haffkine's 
method), consisting of an emulsion of 
killed bacilli, has been variously 
practiced without definite result as 
yet. 

9. BACILLUS COL! COMMUNIS gener- 

ally spoken of as Bacillus of the "coli 
group" in as much there are various 
bacteria which are closely allied to 
one another and some with different 
names which are probably identical. 
The bacillus coli communis is an or- 
ganism that greatly resembles the 
typhoid bacillus. 

It is normally found in the gastro in- 
testinal tract and biliary passages. 
It seems to benefit the body in that 
it restrains, to a certain extent, the 
growth of putrefactive and possibly 
pathogenic organisms. In certain con- 
ditions of the body it develops rap- 
idly and increases in virulence, and 
when it wanders from its proper 
habitat into damaged tissues it is cap- 
able of producing Inflammatory or 
suppurative conditions. It is found 
in various diseases, the gastrointesti- 
nal track, biliary passages and 
urinary system such as cystitis, 
pyelitis and pyelonephritis and of 
other viscera, also in peritonitis, from 
the escape of the bacillus through the 
intestinal wall or a ruptured intestine 
or secondary to enteritis, pleurisy, 
endocarditis and other inflammatory 
diseases. 

10. BACILLUS PARATYPHOSUS or 
PARA COLON GROUP is closely al- 
lied to the typhoid and coli com- 
munis, though they differ in some es- 



98 PATHOLOGY. 

sential particulars. 

Para colon or Paratyphoid infection has 
been described, as resembling typhoid 
fever clinically, by several writers, 
but the tendency at the present time 
is to regard it as distinct in a bae- 
teriologic sense rather than in a clini- 
cal or pathological sense. 

The classification of paratyphoid in- 
fection as a subvariety of typhoid in- 
fection is probably warranted. 

11. SPIRILLUM CHOLERA ASIATICAE, 

Asiatic cholera spirillum, Vibrio chol- 
era asiaticae, Koch's comma baccillus, 
is found only in the intestinal contents 
and mucosa and produces the "rice 
water" stools of choleraic patients. 
The intestine shows congestion fibrin- 
ous inflammation and necrosis. 
The toxins absorbed from the bowel 
give rise to the extreme toxemia with 
congestion and necrosis of the 
viscera. 

The rapid and copious intestinal dis- 
charges lead to inspissation of the 
blood and the collapsed appearance 
invariably found. 

Protective vaccination gives encourag- 
ing results. 

12. BACILLUS MALLEI, Bacillus of 
glanders, is the specific cause of the 
inflammatory infection of the nasal 
mucosa called glanders, in horses and 
asses which is sometimes communi- 
cated to other animals and man. The 
organism resembles the tubercle 
bacillus to a certain extent. 

The mucosa of the nose is characterized 
by its slightly elevated nodules at 
first, these later show a marked tend- 
ency to soften and become irregular 
ulcers. The lymphatic glands of the 
neck, and elsewhere, enlarge and sup- 
purate. It may attack the skin but 
the lesions here are more sluggish. 

In man, similar nodules and ulceration 
may be found in the nose, larynx or 
trachea. The skin is attacked in the 
form of pustules, boils and abscesses. 

Nodules may also form in the viscera 
and there may be arthritis and 
ostemylitis. 



BACTERIA. 99 

13. BACILLUS OEDEMATIS MALIGNE, 
Vibron Septique, Bacillus of malign- 
ant edema. The bacillus resembles 
that of anthrax, but more slender. 
It is the specific cause of an intense 
infection causing 1 inflammation and 
is called malignant edema, which is 
seen in certain animals and man. 

The bacillus occurs in the subcutaneous 
tissues near the point of entrance, 
also in the muscles and peritoneal 
cavity at the time of death. 

It is not found in the blood as it is 
anaerobic. 

The subcutaneous tissues undergo rapid 
supperation and necrotic inflammation 
with rapid emphysema and gangren- 
ous alterations and pus formation or 
extensive hemorrhagic infiltration. 

14. BACILLUS ANTHRACIS, is a strepto 
bacillus, the specific cause of anthrax. 
It occurs most frequently in cows 
and sheep. 

In animals it is called spleenic fever; 
in man malignant pustule and wool 
sorters disease. The mode of infection 
in animals is most frequently the 
gastrointestinal tract, the microor- 
ganism being swallowed with the food. 
They may, however, gain entrance 
through the lungs or, which is most 
common in man, through external 
abrasions. The bacillus occurs in all 
the local lesions and from these 
they are carried to the blood and or- 
gans such as spleen, liver, kidneys 
and lungs. 

The lesions produced by anthrax are 
more or less local but occasion a gen- 
eral septicemia. When infected 
through abrasions of the skin, the 
inflammatory process is intense, the 
areas are often covered and sur- 
rounded by bulbous vesicles and at- 
tended with edema, 

The surface may become eroded with 
discharge of sanious liquid and crust 
formation. 

When infected through the gastro- 
intestinal tract, the mucosa and sub- 
mucosa is affected like the above. 
The lesions are first hemorrhagic, 
then swelling follows, ulceration of 



100 PATHOLOGY. 

surface and profuse diarrhoea with 
discharges may occur. 

When infected through the lungs, the 
bacilli lodge in the alveoli, rapid cel- 
lular exudation with edema and 
hemorrhagic infiltration follows. Sero- 
sanguinolent pleurisy, enlargement of 
the mediastinal glands and some- 
times a hemorrhagic extravasation in- 
to the mediastinal spaces occurs. 

15. BACILLUS AEROGENES, is an ana- 
erobic bacillus which somewhat re- 
sembles the bacillus of malignant 
edema. It is about as thick as the 
bacillus of anthrax, adjacent ends are 
slightly rounded or square and it oc- 
curs singly, in pairs, clumps or short 
threads. 

It is the specific cause of Infectious em- 
physema (gaseous gangrene, gas- 
phlegmon, emphysematous necrosis). 

Infection takes place through some in- 
jury or abrasion. It has been met 
with during the puerperium, probably 
from uterine infection, and it is prob- 
able that many cases of air-embolism 
from douching the uterus after la- 
bor are realy this form of infection. 

The lesions are wide spread. At the 
point of entrance there is edematous 
infiltration with bloody fluid and 
emphysema due to gas formation. 
Necrosis and gangrenous softening of 
tissues occur rapidly. The entire sur- 
face of the body may become 
emphysematous as does the my- 
ocardium kidneys, liver and spleen. 

The blood of the heart and vessels pre- 
sent a foamy condition, due to gas 
formation. 

The bacilli are found in the gas vesicles. 

16. ACTINOMYCES BOVIS. Ray-fungus, 
is an anaerobic organism. The specific 
cause of "Lump Jaw" in cattle and 
horses, it also infects man. 

The streptothrix, cladothrix, etc. was 
at one time classed as this organism 
but this has been disproved, as they 
are aerobic. 

The manner of infection has not been 
determined. In the tissues affected 
there is round-celled infiltration, and 
proliferative changes in. the connect- 



BACTERIA. 101 

ive tissue surrounding 1 the organism 
with sometimes secondary softening, 
necrosis or suppuration. The granu- 
lation tissue is rich in leucocytes 
and foci with purulent collections 
may develope. 

In cattle the disease affects the lower 
jaw more often than the upper or 
other bones, the tissues of the neck, 
tongue, etc. 

In man it is seen in the gums, cheeks, 
mouth, lungs, intestine and the other 
internal organs. 

The lesion is first a hard red papule 
which increases and later breaks 
down forming necrotic or suppurative 
excavations. Scar formation may ex- 
tend to some parts while the necrosis 
may go on in other directions, so that 
irregular cavities are established. 

In the pus or necrotic tissues the so- 
called sulphur granules of the or- 
ganism are found. The disease tends 
to become limited or retarded and 
sometimes this is completely effected. 

17. STREPTOTHRIX MADURAE, is an 

organism somewhat allied to the 
actinomyces. and is the specific cause 
of mycetoma or madura foot of In- 
dia. It affects the foot, and its mode 
of infection is generally by injuries 
from thorn wounds, etc. The hands 
or other parts are rarely affected. 

There is first a nodular swelling which 
spreads. Later there is softening 
with rupture and a discharge of thin, 
watery pus containing grayish or red- 
dish granules or black granules like 
gun powder. 

In the later stages, discharging sinuoses 
may remain. New nodules are form- 
ed and softened, the affected mem- 
bers are greatly deformed. Death 
occurs from exhaustion. 

18. BACILLUS TETANI, is a rod-like 
anaerobic bacillus, frequently swollen 
at one end due to the presence of a 
rounded spore. It is the specific cause 
of Tetanus. The' organism is fre- 
quently found in garden earth, in- 
testinal discharges of animals, and 
articles about stables. 

Mode of infection occurs through 



102 PATHOLOGY. 

puncture made by nails, splinters and 
the like. 

There is no characteristic lesion. The 
germ generally remains at the site of 
inocculation and here produces its 
toxina which are called tetano- 
spasmin, the most prominent and 
causes the spasm; tetanolyism a 
hemolytic substance. 

There is a vascular congestion, chroma- 
tolysis of the spinal ganglion cells 
and death. 

An antitoxin has been prepared and 
successfully, but the disease is gener- 
ally so far advanced before it is 
recognized as to render the antitoxin 
nearly useless. 

19. SPIROCHAETAE OBERMEIERI, is a 
spinal organism found in the fresh 
blood, and is the specific cause of 
Relapsing fever (typhus recurrens). 

The germ is found in the blood during 
the attack, but not during the inter- 
mission. The spleen is congested and 
greatly enlarged, frequently present- 
ing areas of anemic infarctious and 
nercrosis or fatty degeneration. 

20. BACILLUS OF INFLUENZA, Peiffer's 
bacillus, is an extremely small and 
usually single bacillus which is the 
specific cause of Influenza or La 
Grippe. It occurs in the sputum. 
There is no specific lesion. 

There is an intense catarrhal processes 
and at times a pneumonia. There is 
sometimes inflammatory lesions and 
hemorrhagic infiltrations in the mem- 
branes of the brain. 

21. PLAGUE BACILLUS, is a small mo- 
tite bacillus, somewhat resembling the 
bacillus of influenza. 

It is the specific cause of the Bubonic 
plague or pest. The bacillus is found 
in the lymphatic glands, buboes, blood 
and the various organs of those 
affected with the disease. Rats, flies, 
etc. die during epidemics and help 
to spread the disease by infecting the 
soil and dust about dwellings. 

Infection in man is most frequent 
through injuries of the skin such as 
scratches, etc, though it may occur 
through the lungs. 

The lymph glands are attacked and 



BACTERIA. 103 

suppurate (bubo), taking place prin- 
cipally in the inguinal or axiliary 
regions (bubonic type), or secondarily 
at the root of the lungs through a 
primary brouchopneumonia (pneumon- 
ic type), or a general septicaemic 
type, here suppuration is not so com- 
mon. 
Haffkine's preventive inoculations have 
been used with good results. 

22. OIDIUM ALBRICANS, is a budding 
fungus which is the specific cause of 
Thrush in new born infants or in 
older children. The disease is char- 
acterized by a milk-deposit on the 
mucous membrane of the mouth. 

The organism is found in the air and 
various articles of food. 

23. LEPTOTHR1X BUCCALIS, is norm- 
ally found in the mouth and occas- 
ionally penetrate and multiply in the 
crypts of the pharynx, producing a 
chalk-like nodule or deposit. It may 
cause secondary inflammation. 

24. BACILLUS OF TUBERCULOSIS, is 

a rod-shaped organism often occur- 
ing in pairs, arranged end to end 
but not attached. It may appear 
straight or more or less curved and 
may branch. It is found in man, 
cattle and fowl, and is the specific 
cause of Tuberculosis in its various 
forms. The organism may be said to 
be divided into a "human" (which is 
described above) and a bovine bacil- 
lus which is shorter and thicker than 
the human and does not exhibit a 
curved or branching form, which is 
common in the human. 

The tuberculin of the bovine is alka- 
line, in reaction while that of the 
human is strongly acid. It seems 
likely that the human, bovine, avians 
and other animal species of tubercu- 
losis are simply variations of one com- 
mon organism. 

The organism probably occurs and 
multiplies only in the body and 
excreta of diseased individuals. The 
sputa or other excreta containing the 
bacillus may dry and retain the 
bacillus in a dormant state which is 
still potential. It is also found 13 



104 PATHOLOGY. 

the lesions of all parts of the body. 
The mode of infection is generally by 
direct inoculation or by the inhala- 
tion or the swallowing of germs, or 
by intra uterine transference through 
the placenta. 

When the tubercle bacillus is received 
into a tissue or organ, it being a 
foreign body, it acts as an irritant 
to the tissues which react and the 
so-called tubercle is formed. 

With the appearance of the germ into 
the tissues, there is a polynuclear 
leucocytosis into the area from the 
neighboring vessels, together with a 
development of epithelioid cells, which 
look like epithelium, from the fixed 
connective tissue cells or the endo- 
thelium of the lymphatics or blood 
vessels. Some of these cells, either 
by union, or the proliferation of their 
nuclei with a growth, but not a di- 
vision of their protoplasm, form giant 
or myeloid cells which are inclosed 
in a structureless intercellular 
stroma produced by themselves. 

The tubercle formed is of a grayish 
somewhat translucent pearly body and 
is called the miliary tubercle. It is 
avascular and in its further evolution, 
hyaline degeneration, coagulation 
necrosis, fatty change, and finally 
a transformation into a cheesy mass, 
the so-called caseous necrosis (now 
yellow in color) takes place. 
All this is due to a specific action of 
the living bacillus, and in part to the 
avascularity of the tissues. 
The giant cell, although very conspicu- 
ous, is not characteristic of tubercu- 
losis as it is found in many inflam- 
mations, foci of chronic irritation 
and tumors. 
The giant cells are early victims to the 

necrosis. 

When the infection is slight and the 

individual is resistant, the tubercle 

undergoing complete necrosis and is 

;. transformed into a cheesy mass, the 

:;-. surrounding connective tissue may 

* : 4- eventually cause encapsulation of the 

. ...tubercle, and if calcification of the 

..". "-.cheesy, mass ensues, there may be a 




m m 






Fig-. 20. Melanosarcoma, mainly 
round-celled; from a nodule in the skin. 







Fig-. 21. Giant-celled sarcoma. (War- 
ren.) 



*>*:# v 







Fig-. 22. Miliary tubercles in the liver, 
showing- abundant round cells in the 
peripheral parts, epithelioid and giant 
cells within. 




Fig*. 23. Tuberculous lymphatic glands 

a, lymphadenoid tissue; b, largre round 
cells (epithelioid); e, large spindle cells. 
(Ziegler.) 



TUBERCULOSIS. 105 

permanent arrest of the activity in 
the nodule. This is often seen post- 
mortem, the patient having died from 
some other cause. If, however, in the 
necrosis, cavities, sinues, fistulas and 
ulcers are formed, these conditions 
are difficult to heal, or when during 
this condition, breaking down is com- 
mon, it infects the contiguous sur- 
faces or distant organs by means of 
the lymph or blood vessels, the bacil- 
li are thus introduced into the cir- 
culation, an acute fatal infection oc- 
curs which is known as general 
miliary tuberculosis, seen on section 
of the various organs. 

Besides the tubercle there are inflam- 
matory lesions which occur between 
the tubercles and vary according to 
the anatomic character of the parts 
affected. 

In the lungs, the tubercle may be in- 
conspicuous, while the infiltrated lung 
tissues, surround the tubercles and 
filling in the spaces between them, 
gives the organ a definite appearance. 

An inhalation of a considerable number 
of tubercle bacilli may be followed by 
a rapid pneumonia without any tub- 
ercular formations. 

The caseous change is important in that 
liquefaction and cavity formation 
may result which is particularly fre- 
quent in bones, skin, glands and kid- 
ney. 

Frequent seats of tuberculosis are the 
lungs, lymphatic glands, bones and 
joints, mucous membranes of larynx 
and intestines, serous membranes, 
prostrate, testicle, ovaries, fallopian 
tubes, kidneys, uterus, suprarenal 
capsules, brain, liver and spleen. In 
some of the latter sites it is prac- 
tically always secondary. , 

Latent Tuberculosis. A lesion may be- 
come encapsulated and limited, and 
remain so for years without giving 
rise to clinical symptoms, will sub- 
sequently break through its capsule 
and give rise to wide spread infec- 
tion, local or general. Such is seen 
in the post bronchial glands, etc. 

Lupus Vulgaris is a chronic tubercu- 



106 PATHOLOGY. 

losis which affects the skin in its 
entire depth. Wide and ugly 
cicatrices are often formed gradually. 

Scrofula or Struma formerly looked up- 
on as a distinct disease predisposing 
to tuberculosis is now known to be 
tuberculosis occuring in different 
forms and situations. 

Pseudo tuberculosis or false tubercle is 
a condition which resembles the real 
tubercular nodule but is caused by a 
non infective irritant. 

25. BACILLUS LEPRAE is a bacillus 
which closely resembles the tubercle 
bacillus and is the specific cause of 
leprosy, (Lepra or Elephantiasis 
Graecorum). 
The microorganism is found in the lep- 
rous lesions and in the nasal mucus. 
In the tissues. The germ is found 
within the large cells of the specific 
granulation tissue (lepra cells). 

Leprosy occurs in two forms 

a. Tubercular or lepra tubercularis is 
found as small or large nodular ele- 
vations in the skin of the face and 
the extensor surfaces of the arms 
and limbs, etc. 

These nodules are at first reddish in 
color with some inflammatory re- 
action. 

Later the redness is lost and slow 
growing or stationary indolent les- 
ions result. 

They may become ulcerous and do 
not heal readily, or they may be 

converted into cicatrices which 
causes great deformities. 

The appearance of the face is char- 
acteristic and is known as leontiasls 
leprosa. 

The mucous membrane and some of 
the internal organs may be involved. 

b. Anaesthetic form is very insiduous 
in its onset and attacks the con- 
nective tissue and peripheral nerve 
fibers. 

In this form the lesions are less con- 
spicuous, but symptoms such _ as 
hyperesthesia and neuralgic pains, 
with later ulcerations partly trophic 
in nature. Interference with the 
trophic influence of the nerves lead 



SYPHILIS. 107 

to ulceration with loss of the parts 
below the lesions. 
There are whitish or brownish spots 
in the skin which may be slightly 
elevated. 

The anaesthetic and the tubercular 
varieties are commonly coexistant. 
The nodules appearing in the liver, 
spleen and testes are similar to the 
nodules of the skin. The nodules of 
the lungs, kidneys, intestines and 
of the serous surfaces are held by 
many to be tuberculosis and the 
result of secondary infection. 
Other secondary infections are the re- 
sult of injuries to the superficial 
lesions, admiting pyogenic infec- 
tion. 

The term lepra mutilaus and lepra 
gangraenosa are applied to such. 

The Leproma or lepra nodule resem- 
bles that of tuberculosis in struct- 
ure, but differs in its greater 
vascularity and absence of tend- 
ency to cheesy necrosis. The 
abundant blood vessels and a tend- 
ency to complete organization with 
formation of fibrous tissue is mark- 
ed. 

The bacilli occur within the cells 
and sometimes between them. They 
are in large groups and multiply 
within the cell. The protoplasm of 
which undergoes swelling and de- 
generation. The nucleus is broken 
down and the cell is converted into 
a sac containing the bacilli and 
broken down protoplasm. This is 
called the lepra cell. Giant cells 
may be formed. 

26. SPIROCHAETA PALLIDA is a deli- 
cate, actively motile, faintly retractile 
spiral, long, thread-like organism, 
tapering at both extremities and ter- 
minating in pointed ends. It is al- 
most universally accepted as the 
specific cause of syphilis. It has been 
found in the initial lesions, the sec- 
ondary papules, the enlarged 
lymphatic glands, the mucous patches, 
etc., but not as yet in the tertiary 
lesions nor in patients undergoing 
active treatment. 



108 PATHOLOGY. 

Infection occurs by direct inoculation 
in sexual intercourse, though it may 
be conveyed in many other ways, as 
during surgical operations on syphilit- 
ic patients; in the process of tattoo- 
ing or vaccination, when the saliva 
or vaccine lymph from diseased pers- 
ons was employed; by kissing or the 
use of drinking vessels that have been 
employed by the diseased. 

The new born may be syphilitic by reas- 
on of the presence of the disease in 
father or mother. 

Syphilis may be divided into three 
stages: 

a. Primary lesion, the hard indu- 
rated or Hunterian chancre, appears 
in from 10 to 42 days (average 24) 
after inoculation at the point of 
infection, which is generally the 
genital organs, lip, tongue, tonsils, 
pharynx, examining finger, etc. 

It begins as a red, inflamed papule 
or as a vesicle, which ruptures and 
produces an erosion. 

When it appears as a papule the sur- 
face becomes eroded and super- 
ficial ulceration follows. 

The lesion is very hard or indurated, 
which will distinguish it from the 
soft chancre or chancroid. 

Microscopically, the lesion at first 
presents small areas of round cell 
infiltration in the deep layers of 
the skin or mucous membranes and 
in the neighborhood of blood ves- 
sels. 

The connective tissue proliferates 
and spindle or irregular embryonic 
connective tissue cells mingled 
with round lymphoid cells or sur- 
round foci of the latter. A thicken- 
ing of the blood vessels may be 
seen. The tissue elements are 
usually separated by an infiltrated 
liquid which leads to the primary 
vesicle or erosion. 

The induration is probably due to 
connective tissue hyperplasia, 
sclerosis of the vessels and tense 
infiltration of serous liquid. (• 

b. Secondary lesions make their ap- 
pearance at a variable period of 



SYPHILIS. 109 

time after the eruption of the 
initial lesion, and consist of a 
swelling and induration of the 
neighboring lymphatic glands 
(syphilitic bubo). 
The superficial glands of the entire 
body then become swollen and in- 
durated. At the same time erup- 
tions appear on the skin and mu- 
cous membrane. The skin lesion 
may appear in various forms of 
papules, macules and scaly erup- 
tions, symmetrically arranged on 
both sides of the body and cause 
but little irritation. 

The skin is frequently said to be cop- 
pery. On the mucous membranes 
and neighboring skin the most 
characteristic lesion is the condy- 
loma latum, or mucous patch, which 
appears as an elevated patch with 
superficial erosion or ulceration. 

The surface has a necrotic appear- 
ance. It is similar in its structure 
to the initial lesion. The later 
tendency to connective tissue hy- 
perplasia is less marked than it is 
in the initial lesion. 

c. Tertiary lesions appear gradually 
after the secondary lesion. They 
may be divided into— 

1. Localized lesions, which take on 
the ordinary inflammatory 
changes with a tendency to 
fibrous tissue overgrowth and 
thickening or definite nodules 
(gummata or syphilomata). These 
vary in size from small tubercles 
(miliary gummata) to tumors of 
an orange in size or larger. It is 
hard and frequently elastic. On 
section it may be gelatinous or 
mucoid in appearance, but there 
is nearly always considerable in- 
duration either as a capsular en- 
closure or bands, which extend 
from the center to the periphery. 

The gummata may soften and be- 
come converted into puriform 
collections, or when superficially 
placed suppuration, fatty or ne- 
crotic softening may lead to su- 
perficial ulceration that may re- 



110 PATHOLOGY. 

main, become cicatrized or disap- 
pear by absorbtion. 
2. Diffuse syphilitic changes, in this 
condition may be ranked athe- 
romatous thickening of the in- 
tima of blood vessels, certain 
changes in the liver, spleen, kid- 
neys, heart muscle and nervous 
system. 

The tissues of the affected organ 
are indurated, the connective tis- 
sue shows more or less pro- 
nounced hyperplasia. 

Congenital syphilis may be found in 
the new born or may develop after 
birth. The condition may cause the 
child to die in utero or it may cause 
it premature death. The foetus may 
be macerated prior to expulsion. 
Sclerotic lesions of the organs are 
conspicuous. Superficial lesions of 
the skin as vesicles or bullae, fis- 
sures, etc., are also seen. 

The hereditary form with character- 
istic lesions of the bones, teeth, etc., 
does not show itself till later. 

DISEASES DUE TO UNDETERMINED 
BACTERIA. 

1. SOFT CHANCRE OR CHANCROID is 

an infectious venereal sore occurring 
upon the external genitalia, due pos- 
sibly to the bacillus of Ducrey and 
Urma. Various other organisms, such 
as the streptococci and staphylo- 
cocci, gonococcus and other organ- 
isms, are often associated. 

The condition is usually a simple ulcer, 
with suppurating base and edges, 
which discharges freely, may reinfect, 
the patient in other regions, or it 
may take on a malignant phagedemic 
or serpiginous character. 

The neighboring lymph glands usually 
enlarge and may undergo suppura- 
tion (bubo). 

2. SCARLET FEVER, or SCARLATINA, 

is probably due to a micro-organism 
which multiplies rapidly in the blood. 
This is proven by the rapid, fatal 
cases which show no local lesion of 
any severity. There have been vari- 
ous organisms considered as the 
cause, but none proven to be specific. 



MEASLES. Ill 

Among them were the streptococci 

and protozoan organisms. 
Intense lesions of mucous membranes 

and glands are generally present. 

Suppuration of the glands and severe 

inflammations of the throat, middle 

ear, larynx and trachea, endocaditis 

and pericarditis is quite frequent. 

Diphtheria and pneumonia are not 

rare complications. 
Parenchymatous nephritis is common, 

and focal necrosis of organs is seen 

in fatal cases. 

3. MEASLES, or RUBEOLA, is probably 

due to some micro-organism. A 
bacillus resembling that of influenza 
and a protozoan organism have been 
considered, but not determined. 
A catarrhal inflammation of the faucial, 
nasal and conjunctival membranes 
and the bronchial mucosa are cus- 
tomary lesions. There is associated 
congestion and inflammatory enlarge- 
ment of the lymph glands. Second- 
ary degenerations and focal necroses 
also appear. 

4. MUMPHS. The bacteriology is uncer- 

tain. It is an acute inflammation of 
the paroted or the submaxillary 
gland. It rarely terminates in sup- 
puration or on recovery in indura- 
tion. 

5. YELLOW FEVER, or Typhus Ic- 

teroides, is an infectious disease gen- 
erally transmitted through the bite 
of a mosquito — the Stegomyia fascia. 
The specific organism is undeter- 
mined. 

The bacillus icteroides, once considered 
as the cause, is now looked upon as 
a secondary invader. Various other 
organisms have been considered. 

The liver suffers extensive, fatty de- 
generation and appears mottled on 
section. 

The kidneys undergo parenchymatous 
degeneration with extravasation of 
blood. Hemorrhages of the mucous 
and serous surfaces are frequent, par- 
ticularly of the gastric mucosa. The 
brain and the meninges are con- 
gested. Rigor mortis occurs early. 

6. WHOOPING COUGH. Micro-organ- 



112 PATHOLOGY. 

ism is not determined. Lesions of a 
persistent bronchitis are present, but 
are not characteristic. 

7. TYPHUS FEVER (Ship, Jail, Emi- 

grant fever) is rare and of unknown 
cause. The condition suggests an in- 
tense infection and intoxication. The 
blood is often dark colored and pu- 
trifies rapidly. There may be inflam- 
mation of the lungs and bronchi, cere- 
bral and meningeal congestion, and 
albuminous degeneration of the mus- 
cles, liver and kidneys. The spleen 
is enlarged, often soft and may be 
infarcted. 

8. RABES. HYDROPHOBIA. The causa- 

tive micro-organism is undetermined. 
It flourishes in the saliva and salivary 
glands of rabid animals, chiefly 
wolves, cats and dogs, and is inocu- 
lated by their fangs. The virus 
travels along the nerve sheaths to 
the spinal cord and medulla, in which 
it resides. There is gangliomic cell 
degeneration in the medulla and pons, 
loucocytic congestion of their peri- 
vascular lymphatics and atrophy of 
the pneumogastric nerve. 

9. RHEUMATISM. Acute articular rheu- 

matism is probably an infectious con- 
dition. Its real nature, however, is 
undetermined. Many still consider it 
due to faulty metabolism, but the 
evidence is strongly in favor of Poyn- 
ton and Pains' diplococcus rheuma- 
ticus, which has frequently been dem- 
onstrated in the areolar tissue below 
the synovial membrane in arthritis, 
in endo and pericardial lesions, in the 
meninges, in chorea and cerebral 
rheumatism. 

10. MALTA FEVER, Mediterranean fever, 
Gibraltar fever, Febris Undulans, oc- 
curs along the Mediterranean coasts. 
It is not contagious. The organism 
enters the body through the respira- 
tory and intestinal tract. 

The membrane of the small intestine 
is red, and the solitary follicles and 
Pyers patches are sometimes swollen. 

The mucosa of the large intestine is 
dark red, with small round or large 
irregular ulcerations, causing hemor- 



PARASITES. 113 

rhage. The spleen is enlarged and 
hyperemia 
11. BERI BERI occurs in the tropics and 
sub-tropics. There is a degeneration 
and inflammation of the peripheral 
nerves, punctate hemorrhages of the 
serous surfaces, parenchymatous and 
fatty degeneration of the heart mus- 
cle and enlargement of the liver and 
spleen. 

DISEASES CAUSED BY ANIMAL 
PARASITES. 

1. RHIZOPODA. 

f. AMOEBA DYSENTERIAE is an or- 
ganism made up of a clear, refractile 
ectoplasm and a finely or coarsely 
granular endoplasm, frequently show- 
ing a vacuole and sometimes a nu- 
cleus. It has ameboid movement. 
It is found in the stools of dysenteric 
patients, in the tissues of the bowel 
wall near the dysenteric ulcers and 
also in secondary liver abscesses. 

2. AMOEBA CO LI is less distinct than 

a. the dysenteriae in its ectoplasm, 
endoplasm and pseudopodia. "Vac- 
uoles are usually absent. It has a 
distinct nucleus with well-defined nu- 
clear membrane. It is present in the 
faces in 50 per cent, of healthy per- 
sons. 

3. AMOEBA URINALIS is found during 

cystitis. Other amoeba are found in 
the mouth, especially about the teeth. 

4. CERCOMONAS HOMINIS is an or- 

ganism with a pear-shaped body, 
having a cilia on its small anterior 
end, a flagellum on its broad posterior 
end. It is found in diarrhoeal condi- 
tions, cholera, etc. 

5. TRICHOMONAS INTESTINALIS is a 

granular pear-shaped organism, with 
an anterior blunt end and a posterior 
end that is prolonged into a sharp 
tail. The organism contains one or 
two vacuoles. There are 10 to 12 
cilia situated on one side near its 
anterior end. 
It has been found in diarrhoea. 
& TRICHOMONAS VAGINALIS is small- 
er than the T. intestxnalis. It has 



114 PATHOLOGY. 

from 3 to 4 flagella and 6 or 7 short 
lateral cilia. 
It is found in the vaginal discharges 
of vaginitis and in those of women 
of unclean habits. It may be mis- 
taken, by the inexperienced, for the 
spermatozoon. 

7. TRYPANOSOME, Trypanosoma gam- 
blense is found in the horse and cat- 
tle of the tropics, and is also found 
in the blood of man. 

It is a minute worm-like body, with 
one end drawn out into a flagellum 
and the other end bluntly conical. 
The body is short, thick and gran- 
ular, with an attached undulating 
membrane. A vacuole is found near 
its posterior end. 

It exists in the blood of man for a 
long time without causing any symp- 
toms. It then enters the cerebro- 
spinal fluid and causes the charac- 
teristic symptoms — trypanosomiasis — 
irregular and relapsing fever, con- 
stantly frequent pulse and respira- 
tion; oedema, enlarged and tender 
spleen; emaciation, weakness and 
progressive drowsiness, which deep- 
ens into coma and ends in death. 

It is the sleeping sickness of the 
Congo. 

The transmission of the parasite is 
effected mainly by the bite of the 
tse-tse fly (glossina palpalis). 
8. PARASITES OF MALARIA. The 
parasite gains entrance to the blood 
in the saliva of the female mosquito 
of the genus anopheles, which have 
taken the blood of malarial subjects 
into its stomach, where sexual re- 
production takes place as follows: 
The flagellate form (microgame- 
tocytes) are developed and the 
flagella (microgametes), each con- 
taming one part of the nuclear sub- 
.. stance of the parent cell, are dis- 
" charged, and, moving toward the 
■ other parasites which do not form 
flagella (macrogametes), fertilize 
these by penetrating the body of the 
latter. The fertilized parasites invade 
the tissues, segment and develop a 
. ..:capsule r - then called an oocyst, which 



MALARIA. 115 

contains sporozooits, the result of 
segmentation of the parasite. These 
reach the salivary glands and are 
injected into the blood of the next 
person bitten. 
Three distinct species of the malarial 
parasite have been identified. 

a. Plasmodium vivax is the organism 

of the tertian fever. The cycle of 
development in the blood begins 
with a small hyaline spherule, at- 
tached to or with a red blood cell. 
Pigment particles (melanin, derived 
from altered hemoglobin) appear 
within the parasite. The currents 
in the protoplasm render the pig- 
ment motile. 

The body increases in size and the 
corpuscle containing it becomes 
pale. The body continues to in- 
crease in size to or beyond that of 
the normal corpuscle. They are ac- 
tively ameboid until full grown. 

The pigment collects in the center 
and the organism forms a rosette 
and then divides into 15 or 20 
rounded segments or merozoites 
(new spores). The red cell is de- 
stroyed and the merozoites are lib- 
erated, enter other red cells and 
begin the cycle afresh. Then the 
chill or ague-fit is ushered in. 

The cycle is completed in 48 hours. 

b. Plasmodium malariae is the organ- 

ism of the quartan fever. It dif- 
fers from the P. vivax, in that the 
corpuscle does not enlarge or be- 
come as pale; the pigment is less 
in quantity and usually coarse. 

Segmentation is more regular and 
forms a wheel-like figure with 6 to 
12 merozoites. 

The cycle occupies 72 hours. 

A mixture of the tertian and quartan 
orms yield a daily paroxysm — 
Quotidian fever. 

c. Plasmodium praecox is the organ- 

ism of the estivo-atumnal fever, 
and also of tropical or malignant 
forms. It is smaller than" the other 
forms, with less, but coarse, pig- 
ment. It occupies only about 1-3 of 
the the red corpuscle,, and. . divides 



116 PATHOLOGY. 

into 15 merozoites in 48 hours. Seg- 
mentation taking place generally 
within the spleen, bone marrow, 
liver and capillaries of the brain. 

Gametocytes are a feature in the 
later stage of this type of infec- 
tion. At first they are oval bodies, 
then they become crescents with 
centrally placed pigment. 

Gametocytes are significant of long- 
standing infection. They do not 
form when the infection is recent 
and asexual development is active. 

Changes induced are destruction of 
the red cell with its haemoglobin. 
The haemosiderin resulting there- 
from is deposited in the liver, 
spleen and bone marrow. 

The pigmented spleen is enlarged, 
congested and soft. Phagocytosis 
is present. 

The liver and kidneys show paren- 
chymatous degeneration. 

9. COCCIDUM CUNICULI is a small body 

with a delicate outer coat and a 
tough inner double-contoured cap- 
sule. The body is filled with gran- 
ular material sometimes aggregated 
in the center. Sporulation takes 
place outside of the body. The pro- 
toplasm divides into 4 capsulated 
spores containing granular resting 
body between two cicle-shaped 
daughter-spores. Endogenous spor- 
ulation may take place. The organ- 
ism is sometimes seen in the liver 
of man as cystic nodules, which 
spring from the bile ducts or some- 
times as diffuse involvment of the 
liver with cirrhosis, causing jaundice. 
They have also been seen in the in- 
testines, heart and kidneys. 

10. BALANTIDIUM COLI or PARAMECI- 

UM CO LI is a long, slightly ovoid 
body closely betset with cilia. The 
protoplasm is granular, contains a 
nucleus and two contractile vacubles. 
It is natural in the hog and is some- 
times found in diarrhoeal discharges 
in man. 

11. MOLLUSCUM CONTAGIOSUM or 
EPITHELIOMA CONTAGIOSUM, is 

an infectious disease of the skin and 



VERMES. 117 

appears as white or pink papules. The 
lesions have been found to contain 
bodies resembling coccidia. 

The disease is found on the face, neck, 
chest, gentals or scattered over the 
whole body sometimes on the mucous 
membrane. 

12. VARIOLA (Smallpox) and VACCINIA 

(Cow pox). Various micrococci have 
been assigned as the cause for this 
disease but a protozoan parasite of 
the order sporozoa is now being con- 
sidered gravely. 

All authorities do not agree as to the 
difference of variola and vaccinia. In- 
oculation of man by cowpox confers 
an immunity from small pox. 

There are two stages of the disease, 
the invasion of the blood and the ap- 
pearance of the eruption which is 
successively papular, vesicular and 
pustular with the formation of crusts. 
When it is confined to the epidermis 
no disfiguration results; when the 
true skin is affected, scars with pock- 
marks result. 

There may be secondary hemorrhages 
and inflammation of the mucous mem- 
branes; and parenchymatous degen- 
eration of the liver, kidney and spleen. 

Secondary infections with various 
micrococci or other organisms are 
common and may play an important 
part in pustulation and complications 
as septicemia, pneumonia, hemorrhag- 
ic septicemia, erysipelas, etc. 

13. VARICELLA or CHICKEN POX, is a 
mild exanthem the etiology is even 
less determined than that of smallpox. 

II. VERMES (Worms) 

1. CESTODES OR TAPE WORMS, have 
two stages of existence, the larval 
state, found in one species of animals 
(the Intermediate host) and the adult 
state, usually in another species (the 
host). 

The adult worm is found in the in- 
testinal tract of man and lower ani- 
mals. It consists of a head by which 
the worm clings to the mucous sur- 
face, neck and a body which consists 
of separate links or progolottedes. 
The latter are complete organisms 



118 PATHOLOGY. 

containing a complicated hermaphro- 
ditic genital apparatus which pro- 
duces eggs. These are partly dis- 
charged from the segments, into the 
intestinal tract, through a genital 
pore, but escape into the outer world 
when the ripe segments are separated 
from the body of the worm. 
The egg or ovum encloses an imma- 
ture larval organism which, when re- 
ceived into a suitable host, penetrates 
the tissues and lodges in the muscles 
or organs and forms cysts, the well 
known measles of measly pork, beef 
or fish. This closes the asexual stage 
of its life. They contain a head or 
scolex inverted into a sac, filled with 
a clear watery liquid. 
When the flesh, contaminated with 
larval worms, is eaten, the cysts are 
disolved and the scolex fastens itself 
upon the mucous membrane of the 
intestine and the body of the worm, 
is slowly or rapidly formed. 
Tape worms may exist in the intes- 
tines of man without causing any 
disturbance. 

Frequently digestion is interfered with 
and pain and various reflex conditions 
may arise which may result from the 
worm acting as a foreign body or 
from toxins generaled by the worm 
normally or by its death. 

a. Taenia Saginata (beef tapeworm) 
is transmitted usually singly, to the 
intestines of man by infected in- 
sufficiently cooked beef. The worm 
is from 10 to 20 feet in length with 
100 to 2000 segments which are 
greater in length than breadth 
when mature. The head is 1-12 inch 
in length, containing no rostellum 
and no hooklets, but 4 suckers. The 
uteras is a central canal with be- 
tween 20 or 30 branches. 
Papilla with genital pore is on the 
side of the segment, alternations ir- 
regular. Short oval ova are almost 
mature when discharged. 

b. Taenia Solium, is rare in America 
but common in parts of Europe. It 
is transmitted in numbers to the 
intestine of man by infected in- 
sufficiently cooked pork. The worm 



VERMES. 119 

is from 7 to 10 feet in length with 
700 to 1000 segments which are of 
greater length than breadth when 
mature. 

The head is 1-24 inch in length. 
Rostellum contains 26 or 28 hook- 
lets in double row, 4 suckers. The 
uteras is a central canal with about 
10 branches. Papilla with genital 
pore is situated on the side of seg- 
ments, side alternating. 
The ova are spherical and almost 
mature when discharged, 
c. Taenia Echinococcus, is transmitted 
in numbers to the intestine of the 
dog and wolf by infected viscera of 
sheep. The worm is x ,4 inch in 
length with 4 segments. 
The head is 1-26 inch, about the 
same as that of taenia solium but 
smaller; has 4 suckers. The uteras 
is a wide cavity in the last seg- 
ment. Papilla with genital pore 
is on the side of the last segment. 
The ova are spherical. 

Man harbors the full grown intes- 
tinal worm, but he may also be the 
victim of the hydrated stage, as the 
worm in this stage inhabits the 
intestine of the dog, its eggs may 
accidentally be swallowed by man. 
The larva, set free, will enter the 
veins and become encysted in the 
liver, rarely in the lungs, kidneys 
and brain. 

Here it developes as an ichinococcus 
cyst, made up of an outer coat — ■ 
ectocyst and an inner muscular coat 
with blood vessels — endocyst — from 
which will develope secondary or 
daughter cysts (brood capsules) 
from whose walls scolices grow. 
Sometimes, even granddaughter 
cysts are produced — (echinococcus 
hydatidosus). 
d. Bothriocephalus Latus, rare in the 
United States but common in parts 
of Europe. It is transmitted to the 
intestine of man by insufficiently 
cooked lake fish. 

The worm is from 10 to 25 feet in 
length with 3000 to 4000 segments, 
which are greater in breadth than 
in length. The head is 1-10 inch 



120 PATHOLOGY. 

in length, club-shaped and oval, no 
hooklets, 2 suckers. The uteras is a 
tube, arranged in loops giving the 
appearance of a rosette. The geni- 
tal pore is in the center (ventral). 
Ova are oval with operculum, im- 
mature, develope in the water where 
they swim about. 

This worm, when in numbers, may- 
cause intestinal obstruction. It ex- 
cretes poisonous substances which 
being absorbed are the cause of a 
severe anemia. 
e. Hymenolepis Nana (dwarf tape 
worm), is transmitted to the intes- 
tine of man by means of an insect 
or snail (not certain). It is about 
y 2 inch in length. Segmented. Head 
is round; rostellum contains 22 or 
30 hooklets, situated in a circle. The 
genital pore is on the same side of 
all the segments. The ova are oval. 

2. NEMATODA OR ROUND WORMS. 

a. Ascaris Iumbricoides, common 
round worm, single or in numbers, 
of the small intestine. 

It is transmitted to man from in- 
fected drinking water or food. 
They may migrate to the gall ducts, 
stomach, esphagus, larynx or nasal 
cavities. 

They are light brown in color, and 
have a central mouth, with 3 lips, 
at one end and taper to a point at 
the other end. The male is about 
6 inches in length, the female about 
12 inches. 

They are common in the tropics and 
commonly infest unclean people, 
children, negroes and lunatics. 
Tne eggs are produced in great 
numbers and develope in a month. 
They may cause intestinal ob- 
struction, colic, convulsions and re- 
flex nervous disturbances. 

b. Oxyuris Vermicularis (thread, seat 
or pin worm), is very common in 
man. The male is 24 mm. in length 
and the female 10 mm. 

The posterior end of the male is 

blunt and curved, the female 

elougated. 

The eggs are produced in great 

numbers and are oval or elleptical 



VERMES. 121 

in shape. 

It is developed directly from the 
eggs. When ripe the female moves 
toward the rectum and is expelled. 
It is common in children and may 
cause inflammatory troubles or may 
produce a diarrhoea. A vaginitis 
may also be produced by migration 
of the worm. 

c. Trichinella spiralis, occurs as 
larvae in the muscles or organs of 
man and lower animals. The adult 
type is attained in the intestine of 
man. The male is about 1-18 inch 
in length; the female V 8 inch. At 
the posterior end, there is a refract- 
ive cloaca and two projections. 
The encapsulated larva is eaten 
with insufficiently cooked pork, the 
capsule becomes disolved in the 
stomach and they then mature in 
the bowels in 3 days. The young 
are hatched within the uteras, dis- 
charged alive and pass through the 
intestinal wall into the muscles 
where it coils itself and becomes 
surrounded by a capsule. The 
complete cycle takes place in 18 
days. 

Infection of the bowel is ushered 
in by a violent diarrhoea and vomit, 
with occasional collapse. When in 
the muscles (trichinosis) there is 
fever and severe pains like that of 
rheumatism. 

d. Ankylostomum Duodenale or 
Dochmius Duodenalis, is a round 
worm, the female is over y 2 inch in 
length and , twice the diameter of 
the male which is less than y 2 inch 
in length. 

The head is rounded and armed 
with two perpendicular and 
four incurved teeth with which 
it pierces and hooks itself to the 
duodenal mucosa. It is also cuped 
to act as a sucker. The caudal 
end of the male is expanded. 
The eggs are recognizable by their 
pigmentation within the shell and 
appear in great numbers with the 
stools. If they meet with proper 
conditions, as warm climate and 
damp earth they hatch quicklv 



122 PATHOLOGY. 

and the embryos are set free. 
They now develop and are ready to 
re-enter a human host by penetra- 
tion of the skin and thence to the 
blood vessels and is carried to the 
lung. It here leaves the blood ves- 
sel and undergoes further change 
which enables it to resist the gastric 
juice, enters an air vesicle and then 
by means of a bronchus, the 
trachea, osophagus and stomach fi- 
nally reaches the small intestine 
where sexual characters are as- 
sumed. 

The usual intestinal symptoms fol- 
low its entrance with an addition of 
intense anemia (egyptian chlorosis), 
general wasting and often followed 
by death. 

e. Strongyloides Intestinalis, occurs 
in two forms — Parasitical genera- 
tion (auguilla intestinalis), lives in 
the upper intestinal tract, boring 
deeply into the mucous membrane.* 
Eggs develop and the larvae pass 
out with the feces and develop in 
about 30 hours into the, — 

Free living generation (anguilla ster- 
ocoratis). There are therefore two 
methods of reproduction, that of di- 
rect transformation of the rhabditi- 
form larvae into filariform and then 
into adults and the indirect, through 
the intermediate generation. 
Infection occurs through tainted 
water and food. The embryo may 
penetrate through the skin. 
It is common in tropical countries 
and has recently been found in the 
United States. 

f. Trichocephalus Trichiurus or Whip 
worm, is found in the cecum of 
man and sometimes in the vermi- 
form appendix and small intestine. 
It is very common but does not 
usually cause serious disturbances, 
though it may bring on intestinal 
or reflex nervous symptoms. It is 
about % inches in length, with a 
thin thread-like anterior portion 
and a thicker posterior portion 
which is curled upon itself. * 

g. Filaria or Thread worms, are 
found only in the tropics. 



VERMES. 123 

1. Filaria Medinensis or Dracuncul- 
us Meinensis (Guinea worm), 
gains entrance into the intestines 
of man through small crustaceans, 
which they infest, which are 
swallowed in the drinking of 
water. 

It infests the subcutaneous tis- 
sues and the skin. It may reach 
50 to 80 cm. in length and when 
mature causes abscesses of the 
skin. 

2. Filaria Bancrofti or F. Sanguinis 
horn in is (Hominis Nocturna). 
The female is about Sy 2 inches 
long and about 1-100 inch in dia- 
meter. The male is shorter and 
seldom found. The embryos ap- 
pear in the blood, urine, lymph 
and tissue as thread like struct- 
ures. 

The adult form (male and female 
found together), lives in the 
lymphatics of the legs, scro- 
tum and retroperitoneal glands. 
They occur only during the night, 
unless the patient rests during 
the day. 

They generally appear in the 
blood at about 6 P. M., and are 
most numerous at midnight and 
disappear completely before 7 A. 
M. They may be in such num- 
bers (or their eggs) as to block 
the lymph vessels, causing statis 
of lymph stream with enormous 
overgrowth of the scrotum 
(lymphscrotum, Elephantiasis 

Arabum) and the neighboring tis- 
sues. 

Chyle containing filaria embryos 
may appear in the urine from 
rupture of the lymphatics. 
They also cause haematuria, 
lymph abscesses and chylous hy- 
drocele. 

They are generally transmitted to 
man by mosquitoes sucking in- 
fected blood and dying in drinking 
water, in this way conveying the 
infecton. 

Filaria diurna appear in the blood 
during the day. 

Filaria Persians never leave the 
blood. 



124 PATHOLOGY. 

3. TREMATODES OR FLUKE WORMS, 

are small flat tongue- shaped suctorial 
worms, usually hermaphrodite with a 
blind intestine and a ventral suck- 
ing cup, by which it attaches itself. 

a. Fasciola Hepatica, Distoma Hepati- 
cum or Liver-fiuke, is 15 to 35 mm. 
long and 6 to 20 mm. broad, pointed 
at each end, with 2 suckers on an- 
terior end and a beak-like head. 

It is found in the bile-ducts and gall 
bladder of sheep (sheep-rot), only 
occasionally in man. 

b. Opistrochis Sinensis and Feiinens 
resemble one another and are found 
in the bile ducts and gall bladder 
of domestic dogs and cats, and man 
of foreign countries. 

c. Schistomum Hematobium, Distoma 
Haematobium or biiharzia haemato- 
bia, is found in those living along 
the east coast of Africa. The male 
worm is 12 to 14 mm. in length, 1 
mm. thick. The body, back of the 
large ventral sucker is flattened and 
curved to form a grove in which the 
female is attached. 

The female is 16 to 18 mm. long 
and 13 mm. thick. 
The worm enters the body in larvae 
condition with drinking water and 
when developed is found in the 
portal, splenic, mesenteric, rectal 
and vesicle veins. 

At the seat of location it causes in- 
flammation and ulceration, and 
hemorrhage. 

In the uterus and bladder there is 
inflammation, papillary growths, 
deposits of urinary salts, and ob- 
struction of ureters, with pyelitis, 
etc. 
III. ARTHROPODIA, air-breathing ana- 
mal parasites belonging to the group 
Arachnoidea and insecta are also met 
with in man. 

The purely external parasite, infesting 
the skin are mites, — ich-mite (acarus 
scabiei) female burrows in the skin, 
deposits its eggs and gives rise to itch- 
ing. Eggs are hatched and the 3^oung 
mite continues the process; the louse 
(pediculus) ; bed bug (cimex lectuar- 
ius); and the flea (pulex irritans). 
The internal parasites are 



THE BLOOD. 125 

The larvae (Linguatula Rhinaria) 
form of pentaslonium taenioides, 
which is occasionally found in the liver 
and rarely in the spleen, intestinal 
walls, lung and kidney of man, where 
it creates a small nodular lesion which 
consists more or less of the degener- 
ated parasites lying in an encapsulated 
cheesy or semicalcified mass. 
The adult form lodges in the nasal 
cavities of dogs, etc. and produces eggs 
containing the embryos which pass out 
with the nasal secretions and in this 
way gain access to the alimentary 
tract of man. 

The larvae of various flies are some- 
times deposited in wounds, nasal and 
pharynageal chambers. They develop 
and cause local inflammation which is 
called myiasis. 



SPECIAL PATHOLOGY. 
DISEASES OF THE BLOOD. 

The ERYTHROCYTES or the RED 
BLOOD CELLS in health are 7 to 8 m. 
in diameter and number 5,000,000 per 
c. mm. in man and 4,500,000 in women 
with variations depending upon the 
time of day and the relation to the 
taking of food. 

The WHITE CELLS or LEUCOCYTIS in 
health vary considerably as to number 
but may be averaged between 6,000 and 
8,000 per c. mm. They are classified 
according to their size and the appear- 
ance of their nuclei; more especially, 
however, from their reaction to aniline 
dyes. 

If the cells protoplasm is acid they have 
an affinity for basic stains and are 
called Basophile Cells. If they, on the 
other hand, have an affinity for acid 
stains they are called Acidphile, Oxy- 
phile or Eosinophile cells. 
Those, which react to neither stain, 
but to a mixture of the two, are called 

NeutrophFFe Cells. 

Therefore we have the following classi- 
fication 



126 PATHOLOGY. 

1. Basophiles. 

a. Lymphocytes, constitute about 22- 
25% of the leucocytes, when over 
this, condition is called lymphocy- 
tosis. In size they are about the 
same as that of the red blood cell, 
they contain a large deeply stained 
nucleus which almost fills the cell. 

b. Large mononuclear leucocytes 
constitute about 2-4% of the 
leucocytes. They are about twice 
the size of the red cell. The 
nucleas stains poorly and is sit- 
uated at the side of cell. Transit- 
ional forms show neutrophilic 
granules with lobing of the nucleus. 

c. Mast Cells, constitute about 0.5% 
of leucocytus. They may vary in 
size and have va*rious shaped nuclei. 
Their basophile granules are heavily 
stained. 

.2 Neutrophils constitute about 70 to 
72%) of leucocytes. They are poly- 
nuclear or polymorphonuclear. The 
nucelus stains deeply. 

3. Eosinophiles constitute about 2 to 4% 
of leucocytes. They vary in size from 
that of the red cell to the large 
mononuclear cell. They have amoe- 
boid movement. Bilobed nucleus 
takes the stain faintly. Protoplas- 
mic granules takes the stain strong- 
ly. 
PATHOLOGIC FORMS OF THE BLOOD 

CELLS. 

1. THE RED CELLS. 

a. Microcytes, are 1-4 inch in diamet- 
er, undersized and poor in haemo- 
globin. 

b. Megalocytes, are 10-20 inch in di- 
ameter, oversized, deficient or rich 
in haemoglobin. 

c. Poikilocytes, irreguarlity of form. 

d. Erythroblasts, nucleated red cells. 
They are divided into 

1. Microblasts— exceedingly small in 

2. Normoblasts— size of normal red 
cell. 

3. Megaloblasts— large and irregu- 
lar. 



HYDREMIA. 127 

Degenerations of the nucleated red 
cell may occur as 

Karyolysis — solution of the chro- 
matin. 

Karyorrhexis — fragmentation of the 
nucleus. 

Pyknosis — clumping or condensa- 
tion of the nuclear structure. 

Granular degeneration, vacuolation 
and nuclear atrophy. 

Karyokinetic figures. 

e. Shadow corpuscles, cell has lost its 
color. 

f. Ring bodies, are probably the re- 
mains of a previous existing nu- 
cleus. 

THE WHITE CELLS. 

a. Mast cells, are nearly always 
pathologic. 

b. Myelocytes, mononuclear, either 
neutrophilic or eosinophilic, they are 
3 or 4 times the size of the red 
blood cells, with a large, pale, oval 
nucleus, which is placed to one side. 
These cells are identical with the 
large granular cells of the bone 
marrow. 

PLETHORA, is a supposed excessive 
quantity of blood. It has been describ- 
ed as 

1. Plethora Vera, a supposed increase 
in the quantity of blood without any 
change in quality. It is found in in- 
dividuals living in luxury, who have 
a high color and a vigorous circula- 
tion. The term "full blooded" is now 
applied and is probably due to fullness 
of superficial vessels. 

2. Plethora apocoptica, is a local in- 
crease in blood. 

3. Plethora hydraemica, the quanity of 
blood is increased by dilution. 

OLIGEMIA, is a reduction in the quantity 
of blood as seen temporarily after 
hemorrhage. It may also possibly oc- 
cur in certain cachetic and anemic 
diseases. 

HYDREMIA, is a diluted or watery con- 
dition of the blood from excessive 
drinking of water, or hemorrhage, when 
the plasma is rapidly renewed by 
osmosis. 



128 PATHOLOGY. 

ANHYDREMIA. The plasma of blood is 
thickened by a loss of the watery ele- 
ment, as a result of excessive sweating 
or discharge of water from the bowels, 
kidney, etc. 

LIPEMFA. Fat occurs free in the blood 
plasma, normally, to slight extent dur- 
ing digestion and pathologically in 
chronic nephritis, diabetes, pulmonary 
tuberculosis, alcoholism, etc. 

ME LAN EN! A. Dark pigment or granu- 
lar matter appears in the blood as a 
result of maleria and certain fevers. 

HEMOCYTOLOYSIS, HEMOGLOB1NE- 

MIA. Destruction of the red blood cell. 

The haemoglobin is liberated and dis- 
olved in the plasma. 

Causes. It occurs normally in the liver 
where the hemoglobin is changed in- 
to bile pigment. 

Pathologically it occurs in severe 
malaria, relapsing fever, pneumonia 
and hemorrhagic infections and var- 
ious poisons. 

Pathologic Anatomy. The blood is often 
dark in color and shown microcytosis, 
megalocytosis, poikelocytosis, frag- 
mentation and vacuolation. 

Pathologic Physiology. Internal respir- 
ation is disturbed, dyspuora, various 
nervous symptoms, increased coagul- 
ability of the blood and formations of 
thrombi in arteroles and capillaries. 

POLYCYTHEMIA or ERYTHROCYTOS- 

IS, is an increase in the number of red 
cells. It may be 

1. Actual — overproduction, which is rare. 

2. Relative — from a decrease in the 
quantity of plasma as in certain 
cardiac conditions with slow failure of 
compensation; residents of high alti- 
tudes; new born; cases of cholera, etc., 
where liquid discharges is great. 

LEUCOCYTOSIS, is an increase in the 
number of leucocytos above their normal 
relation to the red cells. 
Causes, it occurs 

Normally in the new born, in preg- 
nency and during digestion. 
Pathologically in 

1. Inflammatory and infectious dis- 
eases such as croupous pneumonia, 



ANEMIA. 129 

suppurations, inflammation of ser- 
ous membranes as peritonitis, pleur- 
isy, meningitis and in infectious 
fevers generally except typhoid, in- 
fluenza, malaria and acute tubercu- 
losis. 
2. Cachetic conditions, at end of 
wasting disease, malignant tumors, 
hemorrhage, massage and cold 
baths, medicines. 

Character of the Blood. The number 
of leucocytes may increase moder- 
ately, 10,000 to 20,000 or excessively 
50,000 to 100,000 per c. mm. The 
polymorphonuclear elements are 80 
to 85% or may be 90 to 95% instead 
of 65 or 70%. 

Pathologic Physiology. It is probably 
for protection. 

HYPOLEUKOCYTOSIS or LEUKOPENIA 

is a definciency in the number of leu- 
coctyes, as is seen to a moderate de- 
gree in various diseases such as tuber- 
culosis, typhoid fever, some pneumonias, 
cachexia, inanition, progressive per- 
nicious anemia, etc. 

Authorities do not agree as to whether 
there is an actual leukolysis or a dis- 
turbance in the distribution of the 
leucocytes. 
ANEMIA, literally want of blood, is a 
general term for a variety of conditions 
in which blood is wanting in one con- 
stituent or another. 

The conditions oligocythemia (reduc- 
tion in red cells) and oligochromemia 
(reduction in coloring matter of the 
corpuscel) are usually associated. 
The anemias arise from two conditions, 
asynthesis (defective formation) and 
haemolysis (blood destruction), and may 
be classified into 
1. PRIMARY ANEMIAS. 

a. CHLOROSIS, "green sickness", is 
due to retarded hemogenesis and is 
characterized by a peculiar pallor of 
the individual and a marked reduc- 
tion of the haemoglobin and occurs 
in young girls and women. 
Causes. 

Faulty developments and want of 
proper hemogenic power. Beginning 
menstruation. Other causes given 



130 PATHOLOGY. 

are heredity, constitutional predispo- 
sition, as poorly developed girls, hy- 
poplasia of the vascular and genera- 
tive systems, emotional excitement, 
homesickness, grief, intestinal intox- 
ications, constipation and menstrual 
disorders. 

Pathologic Anatomy. 

The blood is paler than normal and 
watery. Sp. gr. is low, coagulability 
is increased and number of red cells 
may be normal, but the proportion of 
hemaglobin is decreased in amount. 
In prolonged cases the number of red 
cells are reduced in number, and the 
hemaglobin is from 30 to 20%. The 
cells may be irregular and nucleated. 
Secondary diseases may develop, as 
myocardiac degenerations and dilata- 
tion. The spleen is frequently slight- 
ly enlarged. The skin is yellowish or 
greenish. 

Pathologic Physiology. It resembles 
the secondary anemias so far as the 
general health is concerned. 

b. PROGRESSIVE PERNICIOUS ANE- 
MIA is an anemia which tends to 
increase in severity to a fatal end. 
It shows no deficiency of hemo- 
globin, but an enormous destruction 
of the red cells. 

It occurs in childhood or old age, but 

generally in middle age. 

Causes. Pregnancy, lactation, gastro- 
intestinal disease of various sorts 
from ulcerations to carcinoma, etc., 
and intoxications to the various 
parasites, hemorrhages, systemic 
diseases, as syphilis, malaria, tuber- 
culosis, etc. Depressing emotions, 
fright, exposure and unsanitary 
surroundings act as contributary 
causes. 

Pathologic Anatomy. The blood is 
pale in color, though it may be 
dark. Sp. gr. is reduced. Oli- 
gocythemia progresses rapidly, the 
red corpuscles may sink to 1,000,000 
or less. Microcytes, megalocytes, 
poikilocytes, microblasts, normo- 
blasts and megaloblasts are present, 
with a preponderance of the latter 
form as a rule. Karyokinetic fig- 



LEUKEMIA. 131 

ures and polychromatphilia are 
also present. 

Secondary changes: The marrow of 
the long bones is red, softened and 
often hemorrhagic. The spleen is 
sometimes enlarged. The liver, 
kidneys and heart undergoes fatty 
degeneration, which also frequently 
causes punctate hemorrhages from 
the blood vessels. There may also 
be a degeneration of the posterior 
and lateral columns of the cord. 

There is pigmentation of the liver, 
spleen and kidneys and other or- 
gans from the active hemolysis. 

c. LEUKEMIA or LEUCOCYTHEMIA 

is a disease of the hemogenic organs. 
It is characterized by an increase in 
the number of leucocytes and the 
pathologic changes in the bone mar- 
row, spleen and lymphatic glands. 

Causes. Infection of some nature. 
Diseases such as syphilis, malaria, 
rickets, etc., and probably heredity, 
may be regarded as predisposing 
causes. 

Pathologic Anatomy. 

The blood is light in color. Sp. gr. 
is lowered, the alkaline reactive is 
less decided and coagulation is 
slow. The number of leucocytes 
varies from 100,000 to 300,000 per 
c. mm. in moderate cases to 1,000,000 
or more in severe cases. The nor- 
mal ratio of 1 white cell to 450 red 
may become 1 to 10 or even 1 to 1. 

The lesions of the solid organs occur 
principally in the spleen, bone mar- 
row and lymphatic glands. There- 
fore the terms lienal or splenic, 
medullary or myelogenous and 

lymphatic leukemia are applied. 

Primarily, all forms of leukemia 
probably begin in the bone mar- 
row. 

No sharp distinction can be made 
because the forms are generally 
mixed, but as a suggestion to the 
tissues most affected leukemia may 
be divided into two types — 
1. Splenomedullary or Splenomye- 
logenous or Myeloid form shows 
changes in the spleen and the 



132 PATHOLOGY. 

bone marrow. The spleen is en- 
larged and dense from hyper- 
plasia of the Malpighian tufts 
and infiltration with masses of 
leucocytes. 

Hemorrhages, infarction, degenera- 
tion and necrosis may result. 

The bone marrow also shows hy- 
perplasia. The proportion of the 
white cells to the red are 1 to 3 
or 1 to 2 or even 1 to 1. Large 
mononuclear leucocytes predom- 
inate over the lymphocytes and 
the polymorphonuclear elements 
which are also increased. The 
myelocytes are usually present in 
great numbers. The eosinophiles 
are increased, but not in per- 
centage proportion. Mast cells 
are present in excess of those 
found in health. Karyokinetic 
leucocytes are found in small 
numbers. 

2. Lymphatic form or Lymphatic 
leukemia involves the lymph 
glands. These are hyperplastic 
and may enlarge to the size of 
hen eggs. The spleen escapes. 
Leucocytosis is not so marked 
as it is in the myeloid type. The 
lymphocytes predominate. There 
is also an increase in the large 
mononuclear and the polymorpho- 
nuclear also. 

Myelocytes occur in small numbers. 
Nucleated red cells may be pres- 
ent. 

Acute Lymphatic leukemia strongly 
suggests an infectious condition. 
Its duration is from a few weeks 
to a few months. 

Secondary lesions, as lymphoid in- 
filtrations of the liver, kidneys, 
lungs, heart and other tissues, 
are noted in the lymphatic form, 
and secondary degenerations of 
heart, liver and kidneys may re- 
sult. Sclerosis of the spinal cord 
may also be met with. 

Pathologic Physiology. It is progres- 
sively destructive. The blood con- 
tains toxic substances, as xanthin 
bodies and acids. Albumoses are 



ANEMIA. 133 

present. Urine may contain an ex- 
cess of xanthin bases and uric acid. 

d. HODGKINS' DISEASE (Pseudoleu- 
kemia) (see infections) stimulates 
true leukemia in the enlargement of 
the lymph glands, but there is no, or 
a very moderate, increase in the 
number of leucocytes. 

2. SECONDARY ANEMIA, or SYMPTO- 
MATIC ANEMIA, designates anemic 
conditions due to some underlying 
disease. 

Cause. 

Hemorrhage; parasites in the in- 
testine or in the blood; infectious 
diseases; poisons, such as lead, 
arsenic, phosphorous, coal-tar prod- 
ucts, etc.; organic diseases, and 
new growths, and unsanitary con- 
ditions. 

Pathologic Anatomy. The condition 
of the blood varies according to 
the nature of the anemia. In 
moderate cases the number of red 
cells are 4,000,000 to 3,000,000 per 
C. mm., with the haemoglobin 
correspondingly reduced. In the 
graver forms the red cells are 
decreased to 2,500,000 or 2,000,000 
per C. mm., with the haemo- 
globin very markedly reduced. 
The blood is pale and the corpus- 
cles show various irregularities. 
A small number of nucleated red 
cells may be present. The lymph- 
ocytes may increase relatively 
and actually in severe cases. The 
myelocytes may be present. 
Parenchymatous and fatty degen- 
eration of the heart, kidneys and 
liver may be associated. 

Pathologic Physiology. The con- 
sumption of oxygen and the elim- 
ination of carbon dioxide are nor- 
mal, but to accomplish this more 
active circulation and greater 
energy of the tissues are needed. 
This may cause the degeneration 
of organs stated above and also 
the characteristic symptoms, as 
dyspnoea, palpitations, etc. 

* In the severe forms there is an 
increased tissue waste and 



134 PATHOLOGY. 

greater discharge of nitrogen 
than is digested. 



DISEASES OF THE LYMPHATIC 
TISSUES. 

SPLEEN. 

1. Abnormal Development and Situation. 

It may be absent or there may be 
accessory spleens, or there may be a 
number of small bodies (spleens). 
It may be freely movable as a float- 
ing spleen. In this case a twisting 
of the pedicle may cause its strangu- 
lation. 

2. Vascular Disturbances. 

a. Anemia, from general anemia. The 

spleen is small, firmer and paler 
than normal. 

b. Hyperaemia. 

1. Active during digestion or from 

intense congestion. 

2. Passive, seen in cirrhosis of liver, 

cardiac failure, emphysema or the 
obstruction to large venous chan- 
nels. 

The spleen is large, dark red and 
the capsule is distended; later 
there is thickening of the cap- 
sule and trabeculae, with subse- 
quent contraction, and is then 
called cyanotic induration. 

Hemorrhages, embolism, infarction, 
etc., also occur. Thrombosis of 
the spleenic vein may also occur. 
Calcified thrombi are called 
spleenic stones. 

3. Inflammations, or Spleenitis, may be 

divided into — 
a. Diffuse Spleenitis. Enlargement of 
the spleen occurs during the course 
of infectious diseases, such as 
typhoid, malaria, septicemia, ty- 
phus and relapsing fevers, and to 
less extent in pneumonia, scarlet 
fever, smallpox and influenza. 

There is at first a congestion, and 
if the process advances the spleen 
may become soft. On section it is 
lighter in color than normal. The 
capsule may be distended or 
wrinkled. 



THE SPLEEN. 135 

The cells of the spleenic pulp are 
increased, and there is a hyper- 
plasia of the stroma, trabeculae 
and endothelial cells of spaces. In 
the later stages degenerations may 
become prominent. 

It frequently terminates in complete 
resolution. It may, however, per- 
sist, or frequent infection may 
cause chronic inflammatory hyper- 
plasia, as seen in the so-called 
ague cake spleen of malaria. 

Rupture from distention or suppura- 
tion may also occur. 

b. Circumscribed Spleenitis, or Ab- 
scess of the spleen, may be caused 
by an acute diffuse spleenitis, or 
by an extension from neighboring 
structures, as septic emboli or 
traumatic injuries. 

Abscess may also result from per- 
foration of gastric ulcers or in- 
flammation from other places. 

Small abscesses may be absorbed or 
inspissated with a cheesy or ne- 
crotic residue. Large abscesses 
may be discharged by perforation 
into the stomach or intestines, or 
break into the peritoneal or pleural 
cavities, causing septic inflamma- 
tions of same. 

4. Atrophy of the pulp and proliferation 

of the stroma is met with in old age. 
The capsule is thickened and 
wrinkled. 

5. Degenerations. 

a. Amyloid begins in the Malpighian 
bodies and walls of blood vessels. 
They are pale and grayish in color, 
resembling boiled sago, the so-called 
Sago-grain spleen. 

b. Hyaline, associated with the amy- 

loid and independent of the latter. 

6. Pigmentation results from chronic con- 

gestion or repeated attacks of acute 
spleenitis. 
The pigment may also enter from with- 
out through the circulation. 

7. Calcification in the capsule results 

from chronic snleenitis, infarcts, tu- 
bercular or syphilitic areas and para- 
sitic cysts. 

8. Tumors. Lymphadenoma, primary and 



136 PATHOLOGY. 

secondary sarcoma, secondary car- 
cinoma, endothelioma, cysts, fibroma, 
angioma and lymphangioma. 

9. Parasites, echinococcus, cysts, and 
cysticerci. 

10. Infectious diseases, tuberculosis and 
syphilis. 

LYMPHATIC GLANDS. 

1. Atrophy, from old age and various 

marasmic conditions. 

2. Hypertrophy, very closely allied to 

lymphadenoma. 

3. Degenerations. Patty, amyloid, hya- 

line, calcification, necrosis and pig- 
mentation. 

4. Lymphadenitis, or Inflammation of the 

lymph glands. 

a. Acute is due to irritants being car- 

ried through the lymph channels 
or blood vessels as a result of some 
local or general infection. 

The glands are enlarged and con- 
gested. There is an accumulation 
of leucocytes, a desquamation of 
the cells of the sinuses and an ex- 
udate of lymph. 

It may end in resolution, or when 
the infective cause is of great in- 
tensity necrosis or suppuration may 
occur. 

b. Chronic Lymphadenitis may follow 

from the acute form or from con- 
stant irritation of inhaled particles, 
or digestive disturbances caused by 
improper food, or long-continued 
irritation by particles carried from 
some focus of disease. 

5. Infectious Diseases. 

a. Tuberculosis (Scrofulous glands). It 

appears as small grayish nodules 
within the gland, sometimes with 
hyperemia and inflammation. They 
increase in size and undergo case- 
ous changes. Eventually the entire 
gland is converted into a cheesy 
mass, which may liquefy and dis- 
charge through the ruptured cap- 
sule. 

b. Syphilis. The enlarged glands are 

not so great as those of tubercu- 
losis. They remain hard and do 
not suppurate. In the tertiary 
period gummata (bubo tertiaris) 




Fig-. 24. Tuberculous lymphatic gland; 

a, recent tubercle with giant cell (c) ; 
a, inferior caseous tubercle with giant 
cell (c) ; b, lymphadenoid tissue; d, 
epithelioid cell. (Ziegler.) 



THYMUS GLAND. 137 

may be seen, especially in the 
glands near diseased viscera. 

c. Leprosy and Actinomycosis may also 
involve the glands. 

6. Tumors. Lymphadenoma or lympho- 
sarcoma, primary and secondary sar- 
coma and secondary carcinoma. 

BONE MARROW. 

1. Atrophy, in old age and marasmic con- 

ditions. 

2. Hpertrophy, in anemic diseases. 

The marrow becomes soft and red in 
color. In extreme cases it may be 
dark red and liquid. Fat cells may 
be greatly reduced or wanting and 
various sized marrow cells take their 
place. Pigment cells or red corpus- 
cles and nucleated red cells are also 
seen. 

3. Degenerations. 

a. Fatty infiltration, from general 

obesity, also seen in marantic in- 
dividuals or atrophy of bony tis- 
tues. 

b. Mucoid degeneration and necrosis 

may be part of inflammation. 

c. Pigmentation from blood destruc- 

tion. 

4. Osteomyelitis, or Inflammation of the 

marrow, is of an infectious origin and 
occurs during the course of various 
infectious diseases, or as a result of 
traumatism and direct infection. 

The usual changes met with in inflam- 
mation elsewhere is characteristic 
here. 

The marrow is redder than normal, and 
generally there is punctate hemor- 
rhage. 

The white corpuscles or lymphoid cells 
are increased. Areas of necrosis and 
granular degeneration of cells may 
be seen. The marrow may be puru- 
lent. 
THYMUS GLAND. 

1. Congenital Abnormalities. The gland 

may be absent, irregular or hyper- 
trophied. 

2. Vascular Disturbances. Congestion 

and punctate hemorrhages have been 
seen in death from asphyxia. 



138 PATHOLOGY. 

3. Inflammation. Abscesses from general 

pyemia or extension of suppurative 
affections. 

4. Infectious Diseases. Syphilis, as gum- 

mata in the new born. The gumma 
may caseate and soften so as to re- 
semble an abscess. 
Miliary or caseous tuberculosis may 
also invade the gland. 

5. Tumors. Lymphosarcoma, round-cell 

sarcoma and epithelioma. 

DISEASES OF THE CIRCULATORY 
SYSTEM. 

HEART. 

1. Congenital Diseases and Deformities. 

a. Abnormalities in position and size. 

b. Defective development. 

1. Auriculo-ventricular septa may be 

wanting, etc. 

2. Stenosis and atresia of the pul- 

monary artery, aorta and auricu- 
loventricular orifices. 

3. Defective ventricular or auricular 

septum. 

4. Patulous Ductus Botalli. 

5. Valvular defects, as but two semi- 

lunar valves at aortic or pulmo- 
nary orifices, etc. 
Pathologic Physiology. These con- 
ditions disturb the circulation, 
overfill the venous channels, 
produce an abnormal mixture 
of venous and arterial blood 
and congenital cyanosis and 
morbus coerulens (blueness or 
cyanosis) results. 
Imperfect circulation causes 
thickening of lips and nose and 
clubbing of the finger ends, etc. 

2. Circulatory Disturbances. 

a. Thrombosis of Cavities of the Heart. 
When thrombi are formed some 
time before death they appear as 
deposits upon the heart wall, are 
yellowish or whitish in color and 
are attached between the muscu- 
lar trabeculae. 
Secondary changes of the thrombi, 
as softening, may cause cyst-lil*^ 
cavities to be formed. 



THE HEART. 139 

The thrombi may project from the 
surface in polypoid, form, or they 
may be free ball thrombi or globu- 
lar thrombi. 

The condition may disturb the cir- 
culation by weakening the heart 
muscle or by obstruction of the 
valve orifices. It may also lead to 
embolism. 

b. Thrombosis and Embolism of the 
Coronary Arteries. 

When an embolism lodges or a 
thrombus is formed in the artery 
the area supplied by the artery be- 
comes anemic. The muscular fibers 
of the area becomes white, then 
yellow from softening, and. is called 
Myomalacia cordis. 

Small areas may heal by absorbtion 
with the formation of a scar, which 
may remain or lead to aneurysmal 
dilatation or the rupture of the 
heart may take place. 

3. Atrophy. Seen in advanced age. 

though it may be seen in the young. 
It results from senility and cachetic 
or wasting diseases, as tuberculosis, 
carcinoma, etc. 

The heart is small and the capsule 
is wrinkled and thickened. The ves- 
sels are tortuous. The muscle fibers 
are small and contain pigment. 

4. Hypertrophy and dilatation are usually 

associated and result from the same 
causes, as general over- stimulation 
as in hysteria, exopthalmic goitre, 
etc.; excessive eating and drinking; 
excessive beer drinking, and peri- 
cardial adhesions. 

Sudden strains may cause acute dila- 
tation, and when the heart is de- 
generated the sudden strain may 
cause pure acute dilatation as seen 
in the course of infectious fevers. 

Causes acting on the left ventricle are 
arteriosclerosis, aneurysms of aorta, 
chronic Bright' s disease and exces- 
sive exercise or laborious occupations, 
as blacksmithing, etc. Causes acting 
upon the right ventricle are emphy- 
sema, fibroid phthisis and pleural 



140 PATHOLOGY. 

synechiae. 
Pathologic Anatomy. 

a. Concentric hypertrophy, The 

walls are thickened and the cavi- 
ties are somewhat smaller than 
normal. 

b. Simple hypertrophy. The walls 

are thickened, but the cavities are 
normal. 

c. Eccentric hypertrophy or Hyper- 
trophy with dilatation. The walls 
are thickened and the cavities are 
increased in size. 

d. Pure dilatation, without any hy- 
pertrophy. 

5. Diseases of the Endocardium. 

a. Acute endocarditis, generally affects 
the endocardium of the valves, but 
the endocardium of the cavities may 
also be affected. 

Causes. Various micro-organisms, 
acute rheumatism, scarlet fever, 
pneumonia, puerperal sepsis, Bright's 
disease and malnutrition from carcin- 
oma and nervous affections. 
Pathologic Anatomy. The common 
seats of acute endocarditis in order of 
frequency are the mitral valve, 
aortic valve, pulmonary valve, endo- 
cardium of left ventricle, left auricle 
and right ventricle. 
It may be divided into 

1. Simple or verrucose or beingn en- 
docarditis. First there is an opaque 
area, later small nodules, like beads, 
appear and finally these assume 
wart-like fibrous elevations. 

2. Ulcerative, septic, mycotic, diph- 
theritic, or malignant endocarditis, 
appears as very irrgeular fibrinous 
deposits, or there may be no de- 
posit, or if present it may be de- 
tached and necrosis and ulceration 
of endocardium follows. Secondary 
deposits of fibrin may cover the ul- 
cer or the fibrin may be heaped up 
at the edges of the ulcer. 

The simple form may be healed by 
gradual absorbtion or the breaking 
off of the deposit and its dissemina- 
tion in the circulation. The endo- 
cardium is thickened bv fibro-blastin 



THE HEART. 141 

cells and connective tissue. If the 
process is deep, the area involved 
will be distorted. Large deposits 
may calcify and remain. An entire 
valve or cordae tendineae may be 
destroyed or aneurysms may be 
formed by the penetration of one 
layer only. 

The malignant type affecting the 
endocardium of the cavities may 
lead to myocarditis. 

The most serious danger is embol- 
ism. 

Pathologic Physiology. Acute endo- 
carditis may be the center of disem- 
ination of infectious material, and 
disease may run its course as an 
obscure septicemia. 

b. Chronic Endocarditis, usually affects 
the valves of the heart, distorting 
them, and constitutes chronic valvular 
heart disease. 

Causes. It may continue from the 
acute or it may be chronic from the 
onset as arteriosclerosis and athero- 
ma. Advanced years and laborious 
occupation, chronic alcoholism, gout, 
lead poisoning, syphilis, diabetes, etc., 
are also causative agents. 

Pathologic Anatomy. There is slow 
connective tissue growth in the sub- 
stance of the valves. The valves may 
unite by their surface vegetations, 
causing stenosis, or there may be a 
deposit of lime which causes further 
rigidity. Pieces of the vegetation or 
the calcareous valve may become de- 
tached and cause embolism in other 
organs. 

Hypertrophy of the heart results. This 
of course varies with the condition 
of health and with the seriousness 
of the lesion. If the general health is 
good, there will generally be com- 
mensurately adequate hypertrophy, 
and if the lesion is not sufficient to 
interfere with the circulation of the 
coronary arteries, hypertrophy is well 
maintained. 

Eventually however the heart muscle 
degenerates, the cavities dilate and 
the circulation fails. This leads to 



142 PATHOLOGY. 

changes in the lungs, liver and kid- 
neys. 

Pathologic Physiology. Chronic en- 
docarditis (valvular disease) causes 
more or less profound mechanical dis- 
orders of the circulation, the severity 
depending upon the condition of the 
heart muscle more than upon the se- 
verity of the valve lesion. 
"When compensatory hypertrophy fails 
various organs of the body suffer con- 
gestion. The lungs are first to suffer, 
if the lesion is of the left heart, prop- 
er respiration is prevented and 
dyspnea (cardiac asthma), cough and 
expectoration results. In extreme 
cases, edematous exudation and 
cyanotic induration takes place. 

When the right fails, the liver, spleen, 
gastrointestinal mucosa, kidneys and 
peripheral circulation is congested. 
Metabolic disturbances occur and the 
respiratory exchange of gases is re- 
duced. 

6. Diseases of the Myocardium. 

a. Circulatory Disturbances. 

1. Anemia, from general anemia and 
obstruction of the coronary arteries. 

2. Hyperemia, from obstruction of re- 
turn blood to the right heart and 
failure of compensation in disease 
of heart. 

3. Hemorrhages, from obstruction to 
coronary arteries, intense my- 
ocarditis, surrounding abscesses or 
hemorrhagic diathesis and various 
intoxications. 

b. Degenerations. Parenchymatous or 
cloudy swelling, Amyloid, hyaline, 
fatty infiltration or obesetas cordis 
and fatty degeneration. 

s. Myocarditis or Inflammation of the 
heart muscle, may be divided into 

l.Acute myocarditis, 
a. Acute circumscribed M., or ab- 
scess of the heart occurs in con- 
nection with penetrating endo- 
cardial lesions or associated with 
pericarditis. The infection gen- 
erally takes place through the 
coronary circulation. 



THE HEART. 143 

b. Acute Diffuse M., occurs in var- 
ious forms of infectious fevers as 
in typhoid fever, diphtheria, scar- 
let fever, acute rheumatism, 
puerperal sepsis, etc. 

Under favorable conditions the acute 
diffuse and non suppurative form 
will terminate in resolution. Pro- 
liferative changes, however, are 
likely to advance to organization 
and the formation of localized areas 
of sclerosis. Death may be caused 
by dilatation of the cavities and 
cardiac failure. 

2. Chronic myocarditis or Fibrous 
myocarditis may be diffuse or cir- 
cumscribed. 

Causes. It may be primary but gen- 
erally secondary and is dependent 
upon the interference with the 
coronary circulation and alterations 
in the character of the blood sup- 
ply, as in areas of sclerosis and 
atheroma of the coronary or when 
the blood supply to the arteries is 
interfered with by faulty heart 
valves. 

There is a slow general or local 
production of connective tissue and 
the muscle atrophies and disappears. 

The heart becomes less contractile, 
from the muscular loss and more 
rigid from the increase of con- 
nective tissue, with the degenera- 
tion of muscle fibers, in conse- 
quence of the pressure of the new 
formed tissue, dilatation may take 
place if the area is extensive. 

Angina pectoris, is a paroxysm of 
se^ ere uniform pain which occurs in 
consequence of the fibroid heart. 
This is particularly marked when 
fibroid heart is associated with ad- 
vanced sclerosis of the coronary 
arteries. The cause of the pain is 
uncertain. It may be due to em- 
bolism or thrombosis of the branch- 
es of the coronary arteries. 

7. Infectious Diseases. 

Tuberculosis, occurs as acute mili- 
ary tuberculosis and as caseous 
tubercules from tubercular adenitis. 



144 PATHOLOGY. 

Syphilis, is rare, but gummata may 
be present. 

Actinomycosis, by extension or 
embolism. 

8. Tumors. The primary are rare. 
Sarcoma, fibroma, lipoma, myxo- 
ma and myoma. Secondary are 
more common, sarcomata and 
carcinomata. 

9. Parasites. Echinococcus cysts and 
cysticerci of taenia. 

PERICARDIUM. 
1. Pericarditis. 
Causes. 

a. Primary, are due to irritants car- 
ried by the blood as in rheumatism, 
scarlet fever, small pox, influenza 
and intense septic infections, and 
acute or chronic nephritis. 

b. Secondary, are due to extensions of 
inflammation from the pleura, lung, 
mediastinal glands, sternum, 
esophagus, stomach or the heart. 

Pathologic Anatomy. 

a. Fibrinous or Dry pericarditis. 

b. Serofibrinous Pericarditis. 

c. Purulent Pericarditis or Pyoperi- 
cardium. 

d. Hemorrhagic Pericarditis, seen in 
persons of lowered vitality or those 
suffering from scurvy, purpura, etc. 
The pericarditis accompanying 
tuberculosis or cancer of the 
pericardium is prone to this type. 

Termination. Any of the forms may 
persist for a considerable time with- 
out change. The fibrinous or the 
serofibrinous, after the absorbtion 
of the liquid, variety may produce 
an agglutination of the visceral and 
parietal pericardium, with a grad- 
ual extension of the inflammatory 
process till there is fibrous adhes- 
ions binding the two layers and at 
times with complete obliteration of 
the sac. 

If the inflammation is slight and the 
layers are kept apart by the serous 
exudate the areas of inflammation 
become thickened by new-formed 



THE ARTERIES. 145 

fibrous tissue and sclerotic spots re- 
main upon the surface of the peri- 
cardium and are often called milk 
spots, or portions of the fibrinous 
exudate may remain unabsorbed 
and with the thickened membrane 
suffer calcareous infiltration. 

The purulent form may be discharged 
by rupture, into the esophagus, 
stomach, pleura or even the bron- 
chi, with subsequent adhesions of 
the two layers of the sac. Grad- 
ual inspissation may also take place 
and the cheesy residue may re- 
main or become calcareous. 

Pericarditis may also occasion dis- 
ease of the neighboring structures. 

It is always accompanied by some 
superficial myocarditis. 

2. Infectious Diseases. Tuberculosis, 
syphilis and actinomcosis *may also 
affect the pericardium. 

3. TUmors. Secondary carcinoma and 
sarcoma. Lipoma and fibroma are 
rare. 

4. Parasites. Hydatid cysts and sys- 
tecerci are occasionally seen. 

5. Pneumopericardium, from perfora- 
tion of sac, in fracture of ribs or 
foreign bodies or from the rupture 
of ulcers of esophagus or stomach. 

ARTERIES. 

1. Hypertrophy, as seen in established 

collateral circulation. 

2. Atrophy. Seen in general atrophy of a 

part or from pressure or anemic 
areas. 

3. Degenerations. Fatty degeneration, 

calcareous infiltration, hyaline and 
amyloid degenerations. 

4. Inflammations. 

a. Acute Suppuration or Necrotic Ar- 
teritis. Seen in areas of suppura- 
tive inflammation from extension 
or from lodgment of infected em- 
boli or infection of thrombi within 
the vessel wall. When extension is 
from without, the adventitia and 
then the media undergo round cell 
infiltration and collections of pus 
may be seen in the larger vessels. 



146 PATHOLOGY. 

It may extend to the intima and 
even perforate the vessels and cause 
hemorrhage. 
The suppurative process does not di- 
rectly involve the intima, but leu- 
cocytes emigrate into it and cause 
degenerative changes. 

When the process begins from with- 
in, as through softened thrombi or 
infectious emboli, there is first ne- 
crotic or degenerative destruction 
of the intima and the subsequent 
round cell infiltration of the media 
and adventitia. 

b. Acute productive arteritis occurs 

from thrombosis within the non- 
infected blood vessel and is called 
thrombo-arteritis. It is by this 
means that wounds of vessels, etc., 
are closed. 

It also results from tissue changes 
surrounding the arteries, in diseases 
of organs leading to connective tis- 
sue overgrowth. The condition is 
chronic rather than acute. 

Peri arteritis nodosa, or Arteritis no- 
dosa proliferans, is a rare form 
leading to the formation of fibrous 
nodules. It affects the entire thick- 
ness of the wall and shows nodose 
thickening of the adventitia. 

c. Arteriosclerosis, Endarteritis chron- 

ica deformans, Atheroma, is a 

chronic degenerative and inflamma- 
tory disease of the arteries. 
Causes. It is a physiologic process 
of old age. It generally begins at 
middle life. When it is severe 
and begins early it may be due 
to syphilis, gout, chronic alcohol- 
ism and chronic nephritis. Mus- 
cular exertion, cachexia from 
carcinoma, tuberculosis or in- 
anition. It may follow acute in- 
fections. 

Pathologic Anatomy. 

1. Circumscribed or nodular is com- 
mon in the aorta and large ves- 
sels. Small nodular elevations are 
formed on the inner lining of the 
vessels. They are first of a trans- 
lucent, grayish color and are cov- 



THE ARTERIES. 147 

ered by unchanged endothelium, 
later they degenerate and become 
a dull white or yellowish color, 
then harden with calcification 
(atheromatous plate). It may, 
however, undergo degenerative 
softening and break into the ves- 
sel, leaving a necrotic, ulcerated 
patch (atheromatous ulcer). This 
may now be followed by a cal- 
careous change with fibrinous 
deposits over its surface. The 
sclerosed areas may be few and 
separated, or they may be nu- 
merous and thickly set. 

Microscopically, the nodules con- 
* sist of dense sclerotic tissue. The 
intercellular substance becomes 
hyaline in character, then the 
cells undergo fatty degeneration. 
Then the whole area suffers fatty 
or myxomatous degeneration and 
breaks down into a mass in which 
fat drops and cholesterin plates 
are found. Calcareous material is 
now deposited. 

2. Diffuse affects more or less uni- 
formly a large part of the ar- 
terial system. The changes re- 
semble those of the nodular form. 
There is a widespread thicken- 
ing of the arterial coats, which at 
first affects only the subendothe- 
lia, but later the entire wall. 

In the diffuse form the media may 
suffer fatty degeneration and cal- 
cification with hypertrophy of the 
muscle fibers. A connective tis- 
sue hyperplasia may be seen in 
the adventitia. 

In the nodular form the media is 
usually thinner than normal. 

In the smaller vessels hyperplasia 
of the intima may almost com- 
pletely close the vessels (endar- 
teritis obliterans). The vessels 
may be completely closed by a 
union of the vessel walls or by 
the formation of a thrombus and 
its organization. 

In the larger vessels the loss of 
elasticity by the fibrous tissue 
formation and degenerations may 



148 PATHOLOGY. 

lead to diffuse dilation of the ves- 
sel or localized aneurysmal sacs. 
The vessels may rupture spon- 
taneously. Thrombi may be dis- 
charged into the circulation and 
become emboli. 

Diffuse arteriosclerosis is followed 
by hypertrophy of the heart. 

When small vessels of various or- 
gans are involved degeneration 
and reactive connective tissue hy- 
perplasia results. This is seen in 
softening of the brain and fibroid 
changes in the heart and kidney. 

5. Infectious diseases, syphilis and tuber- 

culosis may also attack the arteries. 

6. Aneurysm is a more or less local dila- 

tation of an arterial wall and may 
be divided into — 

a. False or Spurious Aneurysm, due to 

rupture of the vessel and the en- 
closing of the blood outside the 
artery by an adventitious wall. It 
generally results from trauma. A 
blood tumor or hematoma may be 
formed. When an artery and vein 
are injured the blood may enter the 
vein and distend it .(aneurysmal 
varix). If the artery and vein com- 
municate by an intermediate sac it 
is called varicose aneurysm. 

6. True Aneurysm is the dilatation of 
the arterial walls. 

Causes. Weakened vessel wall and 
blood pressure from any cause. 
It is most common in those whose 
arteries are sclerosed, the causes 
of which may also be given here, 
though a hereditary weakness of 
the arterial coats might also be 
considered as congenital aneu- 
rysms have been seen. 
However, aneurysms appear gener- 
ally at that period of life when 
early senile change and excessive 
muscular exertion overlap one an- 
other. 
Acute degenerative changes may 
also lead to aneurysm. It may 
also result from traumatism. 

Pathologic Anatomy. Aneurysms may 



ANEURYSM. 14'J 

be divided into three varieties — 

i. Ectatic aneurysm is a more or less 
uniform dilatation of all the coats 
of the vessel. It may be fusi- 
form or spindle shaped, cylindri- 
cal and cirsoid (tortuous), the lat- 
ter when seen in the scalp, where 
they stand out prominently be- 
neath the skin, the term anasto- 
motic A. is also applied. 

The intima and adventitia are 
thickened, and there are generally 
atheromatous patches on the in- 
tima. The media is thinner than 
normal and may be wanting in 
some places. 

2. Saccular Aneurysm. A local weak- 

ening leads to the formation of 
a pouch, which frequently com- 
municates with the artery by a 
narrowed orifice. 

The media weakens and gradual 
dilatation of the intima and ad- 
ventitia follow. The sac grows 
larger and larger and rupture 
may take place. A reactive hy- 
perplasia of the surrounding tis- 
sue may act as a secondary re- 
taining wall, and the cavity con- 
tains more or less an abundance 
of clots, which may by their or- 
ganization completely heal the 
aneurysm if it is small. 

In the large aneurysms the sur- 
rounding tissues are pushed aside 
or compressed and may suffer 
necrosis. An aortic aneurysm may 
erode the ribs, sternum and ver- 
tebrae. It may compress the 
spinal cord, or it may rupture 
into various parts of the body. 

Communications may be estab- 
lished with large venous trunks. 

3. Dissecting Aneurysm is common in 

aorta and results from degenera- 
tions and traumatism. The in- 
tima ruptures and the blood bur- 
rows between the coats for a con- 
siderable distance. The dissection 
usually takes place in the media. 
The adventitious canal may be- 
come lined with endothelial 



150 PATHOLOGY. 

VEINS. 

1. Circulatory Disturbances. Thrombosis, 

etc. 

2. Degenerations. Fatty and calcifica- 

tion. 

3. Inflammations. 

a. Acute Phlebitis results from simple 

but particularly infectious inflam- 
mation in the neighborhood of the 
vein. If the outer coat is first in- 
volved the term periphlebitis, as 
seen in Plegmasia albadoiens 
(milk leg), is given. The veins 
show under the skin as blue 
streaks running in various direc- 
tions. 

Cellular inflammation may extend to 
the media and occasionally the in- 
tima, and thrombosis may occur, 
which may become infected and 
cause septic emboli. 

If the condition begins within the 
vein by reason of a primary throm- 
bus the term thrombophlibitis is 
given. If a thrombus is organized 
or partly so calcification may take 
place and phleboliths or vein stones 
are formed. 

Microscopically, the changes are sim- 
ilar to tnose which occur in 
thrombo arteritis. 

b. Chronic Phlebitis, or Phlebosclerosis, 

corresponds to chronic arteritis or 
arteriosclerosis. 

4. Phlebectasia, Varicosity, Dilatation of 

the Veins. 
Causes. Mechanical obstruction to cir- 
culation or weakness of the walls, 
as seen in dependent portions of 
the body as legs, rectum, neck of 
bladder, spermatic cord, scrotum 
and vagina. Cirrhosis of liver, con- 
stipation, pelvic tumors, dilatation 
of veins of rectum, causing hem- 
orrhoids, are frequent. Abdom- 
inal tumors, pregnancy or anything 
causing obstruction to the venous 
return in lower extremity causes 
varicosity of the veins of the leg. 

Pathologic Anatomy. Veins become 
dilated, elongated and assume a 



THE LYMPHATICS. 151 

tortuous character, sometimes 
even pouched. Its walls and sur- 
rounding tissue are thickened by 
chronic inflammation, mechanic- 
ally produced. Rupture may take 
place and lead to fatal hemor- 
rhage. The skin becomes inflamed 
and may break down and pro- 
duce the varicose ulcer. 
5. Infectious Diseases. Tuberculosis and 
syphilis may also attack the veins. 

LYMPHATIC CHANNELS. 

1. Lymphangitis, or Inflammation of the 

Lymphatic vessels, as secondary to 
inflammatory affections of surrounding 
parts. Red lines indicate the position 
and course of the inflamed lympha- 
tics. There is swelling, endothelial 
cell multiplication and later accumu- 
lation of leucocytes within the vessel, 
and the channel may be more or less 
uniformly filled with pus. Peri- 
lymphangitis usually accompanies the 
process, and if the septic process is 
violent phlegmonous inflammation oc- 
curs. : 
Thrombosis may occur and cause ob- 
struction. The process may ter- 
minate in resolution or suppuration 
with involvement of the surrounding 
tissue. The resolution may be im- 
perfect and the connective tissue may 
obliterate the channels, or the walls 
may not be entirely restored and 
dilatation results. 

2. Lymphangiectasia, or Dilatation of the 

Lymphatics. 

a. Acquired. Obstruction by pressure, 

thrombosis or by filariae; inflam- 
mation, as seen in elephantiasis. 
The skin is thickened greatly and the 
surface is lobulated. 

b. Congenital may appear as circum- 

scribed or diffuse forms. The dif- 
fuse appears as edematous swell- 
ings of the subcutaneous and re- 
sembles elephantiasis. 

The localized lymphatic dilatations 
are the same as the new growths 
called lymphangioma. 

3. Infectious Diseases. Tuberculosis and 

syphilis. 



152 PATHOLOGY. 

4. Tumors. Lymphangiomata, endothe- 

liomata and metastatic carcinomata. 

5. Parasites. Filiaria Bancrofti. 
THORACIC DUCT. 

1. Thrombosis in association with inflam- 

mation of duct, sometimes without 
it. This may cause occlusion and 
dilatation of its lower part, also of 
the lymphatics. Chylous ascitis may 
result. Collateral circulation gener- 
ally prevents serious consequences. 

2. Dilatation from cardiac failure with 

engorgement of the greater veins, 
impeding the outflow of lymph. Back- 
ward pressure of the blood through 
the superior vena cava may distend 
the upper part of the duct with blood. 

3. Inflammation of duct is associated with 

various inflammations of the ab- 
domen and pelvis, invasions of irri- 
tants and extension from abdominal 
disease, pleurisy, etc. 

4. Infectious Diseases. Tuberculosis is 

met with. 

5. Tumors. Primary, as sarcoma and 

fibroma, rare. 
Secondary carcinoma is more common. 



DISEASES OF THE RESPIRATORY 
SYSTEM. 

NASAL CAVITIES. 

1. Congenital Abnormalities, deviated 

septum, atresia of parts or complete 
absence of nose is rare. 
Hair lip and cleft palate may involve 
the nasal cavities. 

2. Circulatory Disturbances. Active and 

passive hyperemia, which may ter- 
minate in inflammation in the former, 
and both may cause hemorrhage. 
Hemorrhage (epistaxis) may also he 
caused by inflammation of the mu- 
cous membrane or as a result of 
blood diseases. 

3. Inflammation. 

a. Acute Nasal Catarrh, Acute rhinitis, 
Coryza, results commonly from 
exposure to cold. It may occur as- 
sociated with various infections, as 
influenza, etc. The mucosa is red 
and dry, and a serous, then mucous, 



THE LARYNX. 153 

then muco -purulent exudation is 
discharged. 

b. Chronic Rhinitis follows several 
acute attacks, particularly in the 
scrofulous, tuberculous or syphilitic. 

The mucosa becomes thickened 
(hypertrophic rhinitis), which may 
undergo atrophy (atrophic rhinitis), 
in which the exudate is scanty and 
appears as dry, greenish crusts, 
which may ulcerate and become of- 
fensive (ozena). Offensive dis- 
charges may be due to syphilis 
(ozena syphilitica) or tuberculosis 
ozena (tuberculosa). 

4. Infectious Diseases. 

Diphtheritic rhinitis follows diph- 
theria usually. 

Syphilitis is seen as simple rhinitis con- 
genially and as mucous patches or 
gummata. 

Tuberculosis is seen generally as 
"scrofulous catarrhs" of children. 
Lupus of the face may extend to the 
nose. 

Glanders, leprosy and rhinoscleroma are 
also met with. 

5. Tumors. Polyps, simple generally, but 

fibroid, myxomatous or sarcomatous 
may occur. Chondromata, sarcomata 
and epithelial or glandular cancers 
are sometimes found. 

6. Parasites, Larvae of various flies will 

cause severe inflammation. 

7. Foreign bodies may be encrusted with 

lime salts (Rhinoliths). 

LARYNX. 

1. Circulatory Disturbances. Anemia, ac- 

tive and passive hyperemia and hem- 
orrhage are met with. 
Edema of the epiglottis or other parts 
may be met with in Bright' s or heart 
disease. 

2. Inflammation. 

a. Acute catarrhal laryngitis result of 
irritation, and is associated with 
the various infections. The mem- 
brane is red and swollen. There i. r ; 
a mucous or a muco-purulent se- 



154 PATHOLOGY. 

cretion. In severe forms ecchymosis 
or erosion may occur. It may cause 
disturbance of breathing if severe, 
and children may suffer from spas- 
modic contractions of laryngeal 
muscles with paroxysmal dyspnea 
(false croup). 

b. Chronic catarrhal laryngitis may fol- 

low the acute form or begin grad- 
ually from other irritations. The 
mucous membrane is thickened, 
granular and even papillomatous. 
Fibroid thickening may result from 
irritations of foreign bodies. 

c. Edematous laryngitis, or Edema of 

the larynx, is generally due to in- 
flammations from violent irritations, 
infections, severe chronic local 
lesions of tuberculosis and syphilis 
and perichondritis. 

d. Perichondritis is usually secondary 

to syphilic, tubercular or carcino- 
matous, etc., affections of the 
larynx. 

3. Infectious Diseases. Diphtheritic and 

croupous inflammations as result of 
diphtheria, typhoid fever, scarlet 
fever, smallpox, etc. Tuberculosis, 
syphilis, leprosy and glanders. 

4. Tumors. Papillomatous fibromata, fib- 

roma, carcinoma. 

5. Parasites. Larvae of trichinella 
- spiralis, lumbricoides, echinococcus 

cysts. 

TRACHEA. 

1. Malformations. 

a. Congenital, absence, abnormalities in 
length or diameter or structure. 

b. Acquired. Diffuse or local dilatation, 
constriction from tumors or aneu- 
rysms and cicatricial contraction. 

2. Inflammations are associated with 
laryngitis and bronchitis and are from 
the same cause. 

3. Infe-ctious Diseases. Syphilis and tu- 
berculosis. 

4. Tumors. Ecchondroses and osteomata, 
chondromata and secondary cancers. 

BRONCHI. 

1. Circulatory disturbances, same as 
larynx. 



TRACHEA. 155 

2. Inflammations. 

a. Acute catarrhal bronchitis is due to 

exposure, irritating gases and ex- 
tension of tracheal catarrhs. It is 
associated with typhoid fever, 
measles, whooping cough, etc. It 
may be secondary to pulmonary dis- 
eases, and various micro-organisms 
have been found in bronchitis. The 
mucous membrane is red and dry, 
then a mucous or muco-purulent 
exudate is formed. If the exuda- 
tion is excessive the condition is 
called bronchorrhea. 

It may be serous or purulent and 
very offensive and is then called 
fetid bronchitis. 

b. Chronic catarrhal bronchitis occurs 

from repeated attacks of the acute 
and also in the old or those with 
cardiac weakness. It is frequently 
associated with chronic lung dis- 
ease. 

The ciliated cells are replaced by 
columnar, and the mucous mem- 
brane undergoes hypertrophy. The 
bronchus is thickened by cellular 
infiltration and overgrowth of 
fibrous tissue. 

c. Fibrinous bronchitis is frequently as- 

sociated with laryngeal or tracheal 
diphtheria, but may also be due to 
inhalation of irritants. It occurs 
in the finer bronchi as a result of 
croupous and catarrhal pneumonia. 
The^e is also a form which is char- 
acterized by periodical attacks in 
which fibrinous casts are formed 
and discharged. 

Small spirals (Curschman's spirals) 
containing or associated with them, 
small octahedral crystals (Charcot 
g^id Leyden crystals). 

3, Bronchiectasis, or Dilatation of the 

bronchi, is due to weakness of the 
walls, from chronic bronchitis gen- 
erally, or increased pressure within 
the bronchi or to both. 

When a part of the lungs is atelectic 
the obstruction to the entrance of air 
leads to dilatation above the collapsed 
area. 



156 PATHOLOGY. 

Accumulated secretions in the tubes by 
their weight may sometimes cause 
bronchiectasis. Fibrous adhesions be- 
tween bronchus and pleura may also 
cause it. 

If the dilatation is localized it is called 
saccular bronchiectasis; when it is 
uniformly enlarged it is called cylin- 
drical or fusiform. 

The mucous membrane may be almost 
normal in appearance, but it is gen- 
erally thickened and irregular. There 
may be polypoids and ulcerations. 
The exudation is copious, purulent 
and often fetid. It may sometimes be 
thick and cheesy. 

4. Infectious Diseases. Tuberculosis and 
syphilis. 

5. Tumors. Polypoids, primary cancers, 
leukemic nodules, lymphosarcoma, 
fibroid chondroma and lipoma .may be 
met with. 

LUNGS. 

1, Congenital Disturbances. One lung 
may be absent, or the parenchyma un- 
developed, while the bronchi are in a 
cystic condition. Accessory lobes of 
the lung have been seen. 

2. Circulatory Disturbances. 

a. Anemia from general anemia, pres- 
sure on lung and obstruction to blood 
vessels. The lungs are pale or mot- 
tled in appearance in old people; the 
latter is Cue to pigment. 

b. Active Hyperemia, or Congestion. 

Exercise increases the flow of blood 
to the lungs, and if extreme it may 
cause rapid death (Apoplexia pul- 
monum vascularis). Irritating in- 
halations and Collateral hyperemia 
may occur when the lung or other 
parts of the body become anemic 
through obstruction of circulation 
to the part. 

The lung is dark red and the blood 

will flow from the sectioned sur- 
face. Alveoli may contain free blood 
and it may be seen in the spu- 
tum. 

c. Passive hyperemia occurs from con- 

ditions preventing the outflow of 
Uie blood from the lungs, as in va.l- 



LUNGS. 157 

vular disease or weakness of the 

left ventricle. The hindrance to the 
outflow of the blood in the veins 
leads to similar passive congestion. 
It is found in the dependent parts 
of the lungs in cases of great 
asthenia and is called hypostatic 
congestion. It may lead to hyposta- 
tic pneumonia if irritants are in- 
spired, etc. 

The lung is dark red and heavy. On 
section it is moist, due to an infil- 
tration of serous exudate and blood. 

In chronic cases the tissue is dry 
and indurated. Red and white 
blood cells are found within the 
alveoli and interstitial tissue. In 
later stages the red cell may re- 
enter the circulation or break down 
and remain as pigment granules. 
There is then hyperplasia and in- 
duration of connective tissue, which 
is called cyanotic induration. 

d. Edema, from passive hyperemia, 

general septic conditions, vasomo- 
tor relaxation and stenosis of 
larynx. 
The lungs are dark red when edema 
is due to passive congestion. In 
other forms the lungs are light in 
color, grayish; frothy serous fluid 
exudates on section in both cases. 

e. Hemorrhage. In severe congestion or 

inflammation, hemorrhagic or in- 
fectious diseases and high blood 
pressure small punctate hemor- 
rhages may be met with. 

When hemorrhage is due to conges- 
tion and is mixed with serous ef- 
fusion the lung looks like an hy- 
peremic spleen ((spleenization). 
Large hemorrhages into the lungs 
may result from traumatism or 
aneurysmal rupture. 

Small or large hemorrhages may be 
due to lesions of the nervous sys- 
tem at the base of the brain. 

Hemorrhage discharged externally 
through the bronchial tubes is gen- 
erally due to tuberculosis in its 
later stages. It may occasionally 
be due to congestion of the lungs, 
erosion of small blood vessels by 



158 PATHOLOGY. 

gangrene, abscess, etc., or vicarious 
menstruation. 

f. Hemorrhagic infarcts may occur in 

the lungs as it does in other places 
from obstruction to arteries by em- 
boli. 

g. Embolism without infarction may 

be met with. Traumatic disturb- 
ance of fatty tissue or the break- 
ing of bone may cause a fat em- 
bolism. If large branches of the 
pulmonary artery or several vessels 
are obstructed sudden death may 
result, or there may be only great 
dyspnoea and oppression. 

3. Hypertrophy. True hypertrophy is 
rare. Partial hypertrophy of the lungs 
muscular tissue may occur when there 
is obstruction in air passages so that 
great expiratory force is required. 

4. Atrophy. Occurs only as a part of 
emphysema. 

5. Aatelectasis applies to a non-inflated 
or collapsed lung. 

a. Congenital atelectasis is found in the 

new born in which the lung or 
part of lung has never been prop- 
erly expanded by air as the result 
of general weakness or compres- 
sion of the thorax, or cerebral hem- 
orrhage. 
It may be due to obstruction to the 
air passages by meconium, etc. 

b. Atelectasis in after life, in which 

the lung is compressed or collapsed 
by pleural effusions. deformed 
chests, tumors, aneurysms, etc. It 
is also caused by obstruction to 
the bronchi. 

If the larger bronchi are occluded the 
atelectasis is of considerable ex- 
tent. 

If the smaller bronchi and atelectasis 
are occluded lobular areas of ate- 
lectasis are developed. This is fre- 
quently seen in broncho-pneu- 
monia. 

In some cases the obstruction to the 
bronchi may prevent , inspiration, 
but not expiration, so that there is 
a gradual collapse. In other cases 
both the expiration and the inspira- 



EMPHYSEMA. 159 

tion are prevented with a gradual 
absorption of the air within the 
vesicles. 

Pathologic Anatomy. 

Atelectatic areas are dark in color, 
reduced in size. On section the 
surface is smooth and generally 
dry (called carnification), though 
passive hyperemia may be pres- 
ent and when bloody liquor flows 
from the cut surface the term 
spleenization is given to it. 
The lung does not crepitate and 
sinks when placed in water. If 
the condition has persisted for 
some time the connective tissue 
overgrowth from the septa causes 
induration and permanent col- 
lapse. The lung is then hard, dark 
in color due to pigment of disin- 
tegrated blood. The bronchi may 
be compressed, but sometimes 
atelectatic bronchiectasis may re- 
sult from increased pressure of 
air in the bronchi by reason of 
the collapsed state of the lung 
tissue. 

6. Emphysema is an increase of air con- 
tained within the normal tubes and 
alveoli or in the interstitial connec- 
tive tissue of the lungs. It may be 
divided into, — 

a. Vesicular emphysema, is an over- 
distention of the alveoli and air 
sacs of the lungs. It may be divided 
into, — 

1. Acute Vesicular emphysema, due to 
excessive air pressure within the 
alveoli consequent upon conditions 
such as inflammatory swelling or 
mucous secretions within the 
bronchi, etc., thus impeding ex- 
piration, but not sufficient to ob- 
struct the inspiration and over- 
distention of alveoli and air sacs 
results. 

When the entrance of air into cer- 
tain parts is impeded by obstruc- 
tion, diseased bronchi or pulmo- 
nary consolidation, localized em- 
physema of other parts results, 
this is called vicarious emphy- 
sema. 

Pathologic Anatomy. The alveoli an£ 



160 PATHOLOGY. 

air sacs are simply distended. The 
tissues are paler than normal and 
gives a cotton-like feel when 
pressed between the fingers. 

2. Chronic Vesicular Emphysema, 

Substantial Emphysema, is com- 
mon in old people. Attacks of 
broncho-pneumonia and other in- 
flammatory and congestive condi- 
tions of lungs act as predisposing 
causes. These conditions lead to 
weakness and loss of the elas- 
ticity of the lung tissue. 

The direct exciting cause is prob- 
ably increased air pressure within 
the alveoli by reason of increase 
in expiratory force, as in whoop- 
ing cough, the constant cough of 
chronic bronchitis, blowing of 
wind instruments and constant 
straining in pelvic disorders, etc. 

Pathologic Anatomy. Lung is en- 
larged and often distended, edges 
rounded, light in color, and cot- 
ton-like feel to the fingers. On 
section alveoli are distended into 
cavities of various sizes. When 
large spaces are seen near the 
pleural surface the term bullous 
emphysema is used. The emphy- 
sema may be local or generalized. 

Microscopically, the vesicles and 
alveoli are enlarged and may be 
joined together or the inter-vesic- 
ular and inter-alveolar septa are 
atrophied or destroyed. The blood 
vessels are reduced in number. 

Associated Conditions. The chest is 
in a constant state of inspiration 
(barrel shaped). The diaphragm 
is depressed, the liver is below the 
normal level, and heart is almost 
covered in front and pressed back- 
ward. 

Pathologic Physiology. Obstruction 
to capillary circulation leads to hy- 
pertrophy of the right heart, later 
dilatation of the right ventricle 
and drpsy with cyanosis may re- 
sult. 

3. Senile Emphysema is a result of the 

atrophic process of old age and 
- , is due to thinning of .the inter- 



PNEUMONIA. 161 

vesicular septa. The lung is light 
in color and collapses readily. 

b. Interstitial Emphysema, is air within 
the fibrous tissue of the lung and 
occurs in affections where there is 
obstruction to expiration combined 
with forcible expiratory efforts, as 
severe cough (whooping cough), 
straining during labor or blowing of 
wind instruments, etc., causing the 
rupture of the inter-vesicular septa 
and extravasation of air, which 
eventually passes into the inter- 
lobular and subpleural connective 
tissue, where it appears as small 
movable blebs. The process may 
extend to the root of the lungs, 
mediastinal tissues or subcutan- 
eous tissue of the neck. 
Rupture into the pleural cavities re- 
sults in pneumothorax. 
7. Inflammation or Pneumonia. 

a. Fibrinous, Croupous or Lobar Pneu- 
monia is an acute infection, involv- 
ing a lobe or more of one or both 
lungs, generally caused by the 
diplococcus pneumonia, and is char- 
acterized by a fibrinous exudation 
within the air vesicles and terminal 
bronchioles. 

Causes. Specific cause (see Diseases 
Caused by Bacteria). 

Predisposing causes, — exposure to 
cold, injury to lungs by trauma- 
tism, fatigue and systemic depres- 
sion. 

Pathologic Anatomy. The seat of in- 
volvement is the lower lobe of 
the right lung; lower lobe of left 
lung and apices are less frequently 
involved. There is a tendency to 
involvement of a whole lobe uni- 
f o r m 1 y and simultaneously, 
though it may vary and a more 
or less lobular form may develop, 
or it may spread from one part 
of the lung to another (pneumonia 
migrans. 
-''- Typical cases may be divided into 
the following stages, — 

1. Congestion or Engorgement. 

There is intense congestion with 
exudation of serous liquid and 
blQQ$ corpuscle:-} into the: alveoli 



162 PATHOLOGY. 

and terminal bronchioles. The 
area involved is dark red in color, 
swollen and heavy. There is a 
certain loss of the normal crepi- 
tation. The pleura over the area 
is $ull. On section bloody liquid 
exudes. 

Micraecopically, the blood vessels of 
septa are distended and project 
inward toward the alveoli. Red 
blood corpuscles, some leucocytes 
and detached epithelial cells are 
found in the alveoli. 

2. Consolidation or Hepatization. The 

diseassed part is liver-like, swollen 
and marked on the surface by the 
ribs. On section it is at first red 
in color (red hepatization), later 
white or gray or variegated in 
elderly persons (gray hepatiza- 
tion. The cut surface is dry and 
granular from projecting plugs of 
fibrin. The blood vessels are less 
prominent than in the first stage. 
Leucocytes increase in number. 

3. Resolution. The cells of the exu- 

date undergo fatty degeneration 
and the exudate itself becomes 
gradually softened and the lung 
becomes mo: A st. The material is 
carried off by the lymphatics or 
is expectorated. Puriform liquid 
is present. Crepitation is re-es- 
tablished. 

The epithelial cells of the alveoli 
and bronchioles proliferate, and 
the lung is restored to its previ- 
ous condition. 

In some cases throughout the dis- 
ease there may be severe conges- 
tion and even edema of the lung. 
In drunkards or in the cachetic 
the exudate may be hemorrhagic, 
and in some cases proliferative 
changes in the septa are promi- 
nent. 

Pathologic Physiology. There is gen- 
erally an associated pleurisy. Car- 
diac and respiratory embarrass- 
ment is probably due to the ac- 
tion of toxines on the nervous 
system. In fatal cases white clots 
are often found in the chambers 



PNEUMONIA. 163 

of fhe heart. 

Myocardial degenerations, nephritis, 
albumin and albumosis may be 
sometimes found in the urine. 
The chlorides of the urine are 
usually diminished. The spleen is 
enlarged and soft. Pericarditis 
and endocarditis is common. 
Meningitis may be noted. Inflam- 
mations of the bronchi, larynx, 
stomach and intestines and blad- 
der may be met with. 

Secondary infections may lead to 
abscess or the affected area may 
become gangrenous. Resolution 
may be so delayed and productive 
changes may occur, that a car- 
nification of lung results and is 
then called fibrous pneumonia. 

b. Catarrhal Broncho-pneumonia, Lobu- 
lar Pneumonia, is an acute inflam- 
mation in localized areas of the 
lung tissue in consequence of in- 
flammation of the terminal bron- 
chioles. 

Causes. Some bacterium (diplococcus 
pneumonia in 50% of cases). 
(See Bacterial Diseases). 

It occurs in the course of measles, 
whooping cough, influenza or other 
fevers attended with bronchitis. 
It extends by contiguity and con- 
tinuity or aspiration of irritating 
bronchial secretions. 

Pathologic Anatomy. 

1. Simple Catarrhal Broncho-pneu- 
monia. The pleural surface pre- 
sents areas of dark, light-red or 
grayish color, surrounded by em- 
physema and here and there areas 
of atelectasis. Both lungs are 
generally involved. The small 
bronchi and arterioles contain a 
muco-purulent secretion, and the 
areas of consolidation are smooth 
and moist. The walls of the ter- 
minal bronchioles and alveoli are 
swollen and contain a fluid exu- 
date with disquamated epithelial 
cells. The septa present round 
cell infiltration, and the blood 
vessels are surrounded by emi- 
grated leucocytes. 



164 PATHOLOGY. 

In some cases lobar involvement by 
confluence of the lobular areas 
(pseudo-lobar pneumonia) takes 
place. If the micro-organisms 
are extremely virulent, suppura- 
tion and gangrene may result. 
Fetid foci or purulent collections 
surrounded by areas of conges- 
tion and inflammatory edema may 
result. 

Resolution may be slow, with pro- 
liferation of connective tissue 
and sclerotic hardening, and con- 
traction of the lung tissue re- 
sults. 

2. Hypostatic Pneumonia occurs as a 

terminal affection in many dis- 
eases. It begins as a hypostatic 
congestion and hemorrhagic 
edema of the dependent portions 
of the lungs. Irritants enter 
through the bronchi and inflam- 
mation of the terminal bron- 
chioles and air vesicles results. 
It is more fibrinous than the or- 
dinary broncho-pneumonia and 
the process is more diffuse. 

3. Aspiration Pneumonia. Inhaled 

dust, etc., when it reaches the 
- finer bronchi and bronchioles set 
up a local irritation and conges- 
tion, with disquamation of the 
epithelial cells, and an emigra- 
tion of leucocytes. When the in- 
halation is excessive, as in the 
occupation of coal mining and 
steel grinding, etc., it rarely stops 
with the catarrhal inflammation. 

The irritant penetrates the walls 
and a pneumonia is produced, 
which is more properly a fibrous 
pneumonia. 

c. Cheesy or Tuberculous Pneumonia 

is an acute or subacute pneu- 
monia caused by the tubercle bac- 
illus. 

., V Cause. Tubercule bacillus. It is more 

;.f ■ , common in children than in men. 

V" A tuberculous gland or cavity 

- ruptures into a bronchus and the 

...--■ infective material is disseminated 

!, throughout the lung. The germ 

may be inhaled from without or 



PNEUMONIA. 165 

from foci in the larynx or noso. 

Pathologic Anatomy. It is a lobular 
process. If the infection is 
abundant the areas involved may 
be so close as to resemble the 
lobar form. There is no tend- 
ency to resolution, but, on the 
contrary, it leads to progressive 
cheesy degeneration and the for- 
mation of cavities. Limited areas 
are sometimes healed by reactive 
fibrous overgrowth, encapsulat- 
ing the diseased area and trans- 
forming the whole into a fibrous 
mass. 

. Fibrous Pneumonia, or Productive 
Pneumonia, is a chronic process 
and results from continued irrita- 
tion. It is characterized by over- 
growth of connective tissue, involv- 
ing small or large areas of the lung 
tissue. 

Causes and Classification. 

1. Pneumonokoniosis. Ordinarily most 
of the dust inhaled is lodged on 
the walls of the upper respira- 
tory passages and is discharged 
free with the sputa or in the 
leucocytes and emthelial cells 
(dust cells, Staubzellen). 

If small particles reach the ter- 
minal bronchioles, catarrhal in- 
flammation with proliferation of 
the epithelium and exudation of 
leucocytes is occasioned, which 
may envelop the dust particles 
and remove it by expectoration. 

When the dust inhaled has sharp 
edges, as in coal, iron and marble 
dust, etc., and is in great quan- 
tity, it is difficult in removal. It 
penetrates the walls and passes 
between the epithelial cells and 
occasions a zone of inflamma- 
tory exudation which organizes 
and is enclosed by a fibrous cap- 
sule. 

Some particles float free in the 
lymph or enclosed in leucocytes 
and enter the lymphatic vessels, 
where it may be arrested at vari- 
ous points and occasion fibrous 
thickening of the vessel walls, or 



166 PATHOLOGY. 

produce an indurative enlarge- 
ment of the lymphatic glands at 
the root of the lung and sur- 
rounding bronchi. 

Pathologic Anatomy. In moderate 
cases the lung presents small 
areas of thickening with pucker- 
ing. On section the areas are 
hard and grayish in color. They 
may be darkly pigmented from 
the particles themselves or from 
hemorrhagic pigmentation. The 
fibrous tissue is stellate or con- 
centrically arranged around a 
nucleus of foreign matter. Cal- 
cification is sometimes seen. 

Extensive induration is rare. "When 
met with the vesicular character 
of the lung tissue is lost. Con- 
nective tissue bands follow the 
bronchi and radiate into the 
lungs, which is contracted. Ex- 
tensive adhesions to the chest 
wall often causes deformities of 
the chest. 

2. Secondary Fibrous Pneumonia is 

sometimes seen as secondary to 
the fibrinous or catarrhal pneu- 
monia or atelectasis. It is caused 
by reactive inflammation of the 
septa. It is also seen in some 
cases of caseous pneumonia and 
chronic phthisis. Chronic conges- 
tion of the lung may lead to dif- 
fuse sclerosis of the lung. 

3. Pleurogenic Fibrous Pneumonia 

will follow chronic pleurisy. Tra- 
beculae of fibrous tissue extends 
from the sclerotic pleura into the 
lung tissue. 

4. Peribronchial and Perivascular 

Fibrous Pneumonia is seen with 
the pleurogenic form or the over- 
growth of connective tissue 
around the bronchi and vessels 
which specially results from 
syphilis. 

Moderate forms of this pneumonia 
may occur in association with 
the others. 

e. Purulent Pneumonia is an acute 
form caused by pyogenic micro-or- 



GANGRENE OF LUNG. 167 

ganisms and is characterized by- 
purulent and hemorrhagic exuda- 
tion in the connective tissue, 
lymphatic channels or terminal 
bronchioles and alveoli. The infec- 
tion may reach the lungs through 
the bronchi (Bronchogenic purulent 
pneumonia); the blood vessels 
(Hematogenic purulent pneumonia), 
or the subpleural lymphatics (Pleu- 
rogenic or Lymphogenic pneu- 
monia). 

In the bronchogenic and hematogenic 
forms the pleura is intensely in- 
flamed over the areas and extensive 
purulent pleurisy (Empyema) may 
occur. 

Extensive abscesses may be formed 
which, frequently break into the 
bronchi or sometimes into the 
pleural sac. 

Local or diffuse necrosis or gangrene 
may occur. Recovery may take 
place by absorption or discharge of 
the exudate, but as a rule it is 
fatal. 

In the pleurogenic form there is first 
infection of the lymphatics, and 
then it extends into the lung in the 
form of yellow streaks or bands, 
pushing aside the lobules, which 
gives rise to the term pneumonia 
desiccans. 

Widespread pyemic or toxic lesions 
are often found associated with 
purulent pneumonia; this is gener- 
ally a part of the primary disease. 
Secondary infections as malignant, 
endocarditis, septic nephritis, ett., 
may occur. 

. Gangrene results from putrifactive bac- 
teria in necrotic areas of the lung 
tissue. 

Causes. Extension of adjacent care- 
ous conditions; extension of necrotic 
process of gastric or oesophageal 
ulcers and cancers; inspiration of in- 
fective material from the upper air 
passage; infective material may reach 
.the lung through the blood; pneu- 
monia, tuberculosis and hemorrhagic 
infarction. 

It may appear circumscribed or dif- 



168 PATHOLOGY. 

fuse. In the circumscribed the blood 
vessels escape the gangrenous process 
unless they are occluded by throm- 
bosis, but the bronchi are generally 
penetrated. 

It may extend or a fibrous capsule 
may limit it, and after discharging 
through a bronchus scar formation 
may terminate the disease. 

The diffuse gangrene does not differ 
much except that it is less intense 
and more widespread. Spots of hem- 
orrhagic infiltration, softening and 
formation of cavities may be seen. 
The sputa is muco-purulent. yellow- 
ish gray or brownish in color and 
very fetid. 

9. Infectious Diseases. 

a. Tuberculosis. (See Bacterial Dis- 
eases). 

Infection takes place through bron- 
chial tubes, blood vessels or the 
lymphatic system, hence we have,— 

1. Bronchogenic Tuberculosis. When 
the infective material is inhaled 
and reaches the terminal bron- 
chioles there is set up a limited 
area of caseous or tuberculous 
pneumonia or by penetration of 
the bacilli between the epithelial 
cells, causes tubercular changes 
in the perialveolar and peribron- 
chial connective tissue (miliary 
tubercules). The authorities do 
not agree as to which of these 
processes are more apt to arise. 
It is probable that there is a 
mixture of the two. 

Degeneration soon takes place. The 
areas, beginning as small foci or 
as larger areas of lobular tuber- 
culous pneumonia, change in 
color from a gray to yellow and 
caseate. Coincidently, round- 
cell infiltration and proliferative 
changes take place in the tissues 
surrounding the diseased areas. 

The more acute the disease the 
more apt is the degenerative 
caseation to take place and the 
less likely regeneration to occur. 

In favorable cases the tubercles 



TUBERCULOSIS. 169 

may be encapsulated and con- 
verted into fibrous nodules. 

Varieties. 

a. Acute Pneumonic Tuberculosis is 

more common in children than 
in adults. There must be a high 
degree of susceptibility and a 
great number of virulent bacilli. 

The infection may be derived by 
direct inhalation or be discharged 
from older caseous areas of the 
lungs.. 

Pathologic Anatomy. It is gen- 
erally lobular, but an entire lobe 
may be involved. The base or 
apex may be involved. On sec- 
tion the lung is at first variegated 
from the formation of minute 
patches and lobular areas of 
caseous pneumonia (grayish) and 
surrounding congestion of lung 
tissue. 

The cut bronchiole shows a 
cheesy exudate surrounded by 
peribronchial caseation. Small 
miliary tubercules may be seen in 
edges of the pneumonic patches. 
As the process advances the lung 
tissue is more extensively involved 
and uniformly gray or yellowish 
and consolidated. Complete de- 
struction of the areas take place 
and cavities, appearing generally 
as necrotic excavations, are form- 
ed. The pleura over the lung is 
inflamed and covered with a 
fibrinous or fibrino-purulent ex- 
udate, or it may be studded with 
tubercles. 

If the process is less active there 
may be evidence of reparative 
change. 

Encapsulation of areas and cal 
cification may occur. Fibrous 
overgrowth may convert it into a 
scar mass. Cheesy area, if mere- 
ly enclosed with fibrous tissue, 
may remain quiescent for a time 
and then break through the wall 
and infect anew. 

b. Chronic Pneumonic Tuberculosis 

is the ordinary pulmonary 

phthisis. It generally begins in 

. the apices, though in - children 



170 PATHOLOGY. 

the base of lung is likely to be 
first affected. 

Pathologic Anatomy. If there is 
a bronchitis the bacilli may ad- 
here and cause a tubercular 
bronchitis with ulceration and 
later involvement of the sur- 
rounding tissues. Ordinarily, 
however, the bacilli lodge in the 
bronchioles or alveoli, as in the 
acute form, and cause lobular 
areas of caseous pneumonia sur- 
rounded by tubercles formed along 
the lymphatic vessels and outgo- 
ing from the first formed foci. 
There is a great tendency to in- 
crease the disease by aspiration 
of the caseous material into other 
parts of the lung and by the 
lymphatics. 

On section the lung is found to 
be more or less consolidated in 
areas. These areas are opaque, 
grayish or yellowish in appearance 
and in which can be seen bronchi 
as open spaces filled with a muco- 
purulent liquid. 

Areas of fibrinous or cellular 
pneumonia, which may be due 
to secondary infections, may be 
formed; it differs from the caseous 
in its granular or gelatinous ap- 
pearance and their liability to 
partial or complete resolution. 

A tendency to degeneration and 
softening together with the pro- 
cess of repair may be seen as in 
the acute form. The changes are 
less rapid and connective tissue, 
proliferation and fibrous tissue, 
formation is greater than in the 
acute. 

The necrotic process leads to 
the cavities or vomicae, which are 
characteristic and contain putrid 
secretions, consisting of broken- 
.down, cheesy matter pus cells, de- 
generated epithelial cells, elastic 
tissue fibers, tubercle bacilli, pyo- 
genic bacteria and sometimes 
mold fungi. The cavities are 
formed by bronchiectasis or by 
liquefaction of the caseous areas 
not in connection with a bronchial 
tube. Single cavities may grow 



TUBERCULOSIS. 171 

larger by constant ulceration, due 
not only to caseous tuberculous 
degenration, but also to mixed in- 
fection. The walls of the cavities 
are formed by reparative fibrous 
proliferation and are covered by a 
"pyogenic membrane." Blood ves- 
sels in the areas may show 
aneurysmal dilatation, erosion of 
these will streak the sputum in 
the early stage while rupture of 
the vessels produce the hemorr- 
hage in the later stage. 

Connective tissue formation, en- 
capsulating the area, may limit 
the disease, or it may be com- 
pletely fibrosed, as in, 

C. Fibroid Phthisis, which may be- 
gin before or after the cavity 
formation, tends to counteract 
caseation and destruction. If it 
begins in the early stage a well- 
formed capsule will separate the 
area from the surrounding tis- 
sue, and by its tendency to 
shrink the material may be- 
come calcareous and the dis- 
ease process is completely ar- 
rested. 

If the capsule is not firm the dis- 
ease, after having been quies- 
cent for a varying period of time, 
will be perforated by a fresh 
extension and an acute or 
chronic course of the disease 
will be established. If the foci 
of the disease are minute the 
fibrous tissue proliferation con- 
verts it into a sclerotic mass 
instead of capsule formation. 

Complications of Bronchogenic 
Tuberculosis. Involvement of the 
pleura; swallowing of the sputa is 
liable to produce intestinal tuber- 
culosis; upper air passages may be 
involved; blood dissemination of 
the infection may cause lesions 
of the vessels, pericardium, endo- 
cardium and general miliary tub- 
erculosis; acute pneumonia, and 
hypertrophy of the left ventricle. 

2. Hematogenic Tuberculosis occurs 
when a tubercular focus in the 
cervical or peribronchial lymph 
gland or foci at apices of lungs, 



172 PATHOLOGY. 

etc., rupture into a blood vessel. 
It is a part of general tubercu- 
losis. The organs most frequent- 
ly infected are spleen, liver, kid- 
ney, choroid coat of eye, men- 
inges and most of all the lung. 
Pathologic Anatomy. Is the forma- 
tion of miliary tubercles and their 
acute or chronic changes, etc. 

3. Lymphogenic Tuberculosis. Di- 
rect infection to the lungs may 
take place by means of the lymph 
channels, as in tuberculous 
pleurisy, which may be primary 
or secondary to tuberculous dis- 
ease of the vertebrae or ribs. 
It may also be carried by the thor- 
acic duct from the lymphatic 
glands of the abdomen and pos- 
terior mediastinum and caseous 
vertebrae to the blood vessels 
and then to lungs as a hemato- 
genic infection. 

Pathologic Anatomy. Typical tu- 
bercles are scattered along the 
lymph vessels in the interlobu- 
lar septa and surround the blood 
vessels and bronchi. 

b. Syphilis. 

1. Diffuse syphilitic infiltration of the 

lungs is seen in the "still-born." 
It appears as a more or less lobar 
consolidation and induration of 
the lung tissue. The lung is light 
gray and airless (pneumonia 
alba). 

2. Syphilitic Gummata may be asso- 

ciated with the diffuse form of 
congenital syphilis, or it may be 
present without the diffuse va- 
riety. It is sometimes seen in the 
adult. 

3. Syphilitic fibrous induration of the 

lung has been described. 

c. Glanders. Infection takes place by 
inhalation and rarely through the 
blood. The lesion may be a diffuse 
grayish or purulent infiltration with 
abscess formation, or they may be of 
a nodular character, of the size of a 
hemp seed or a pea, in various parts 
of the lung and show early degenera- 
tion. 



PLEURA. 173 

10. Tumors. Connective tissue tumors, — 
fibroma, lipoma, chondroma, osteoma. 
Sarcoma (primary and secondary are 
more common. 

Epithelial tumors, — carcinoma, the pri- 
mary is the more common, while sec- 
ondary is less frequent; adenoma has 
been described. 

Cysts, — congenital and are probably 
merely dilatatious of bronchi have 
been described. Dermoids are rare. 

PLEURA. 

1. Circulating Disturbances. 

a. Passive Hyperemia, is seen in dis- 
eases interfering with respiration, 
pressure upon azygos vein, and in- 
trathoraic pressure. 

b. Petechial Hemorrhage, is seen in in- 
tense congestion, blood disorders and 
hemorrhage diathesis. 

c. Hemothorax, free blood in the pleural 
cavity from wounds, fracture of ribs 
and rupture of aneurysms. If infec- 
tion does not take place the blood is 
generally absorbed rapidly. 

d. Hydrothorax, or dropsy of the pleural 
cavity, may be a part of general 
edema. It is a serous effusion. Usu- 
ally bilateral but may be unilateral. 
The pleura frequently undergoes some 
opacity and loss of luster. There may 
be edema of the subpleural fibrous 
tissue. Compression of the lungs and 
displacement of adjacent viscera is 
produced. 

e. Pneumothorax, air in pleural cavity, 
from rupture of tuberculous cavities, 
gangrenous areas, softened infarcts or 
abscesses of the lung, or rupture of 
emphysematous air vesicles allowing 
air to enter the pleural sac. 

It may also follow the rupture of an 
empyema into the lung. It may be 
due to penetrating wounds. 
The air is frequently absorbed, but if 
infection takes place, purulent exuda- 
tion from the pleura is caused and the 
condition is then called pyopneumo- 
thorax. The adjacent organs are 
often displaced. 

2. Plexitis, Pleurisy or Inflammation of 
the Pleura. 



174 PATHOLOGY. 

Causes: 

a. Local causes, inflammatory exten- 
sion from the various pneumonias, 
gangrene and tuberculosis; extension 
from pericarditis or mediastinal dis- 
ease and inflammatory affections of 
the spine, ribs or chest walls. 
Inflammatory extension from the ab- 
domen or its organs may take place. 
Perforation of gastric ulcers, etc., and 
abscess of the liver or spleen in rare 
cases may cause it. 

b. General causes, results from infec- 
tion or intoxication reaching the 
pleura from the blood, e. g. pyemia 
and septicemia, rheumatism, acute 
infectious diseases and Bright's dis- 
ease, and acute inflammation. 

Cold and traumatism are predis- 
posing factors only. 

Various microorganisms causing in- 
flammation are met with. 
It may be secondary to pneumonia or 
tuberculosis, or the germs of these 
diseases may be found in primary 
pleurisy without affection of the 
lungs. 
Pathologic Anatomy. There are sever- 
al varieties of pleurisy but one gen- 
erally merges into the other. 

a. Fibrinous Pleuritis. The pleura is 
congested, lusterless and followed by 
a fibrinous exudation. The pleural 
surfaces become agglutinated which 
when separated are roughened so as 
to give rise to the term "bread and 
butter pleurisy." 

This process may involve small areas 
only, or it may be extensive. If 
small areas only are involved ab- 
sorption takes place so that the 
pleura is restored to its normal con- 
dition. If it is extensive organiza- 
tion takes place so that the pleura 
are bound together by connective tis- 
sue, which is later developed into 
sclerotic bands. When it occurs re- 
peatedly, as in tuberculosis, and is 
not extensive, the pleura may be 
thickened in spots from connective 
tissue proliferation. 

b. Serofibrinous Pleurisy may be a sec- 
ondary condition to the fibrinous, or 
it may begin as a serous exudation 



THE MOUTH. 175 

into the sac. The fluid is heavier 
than dropsical and contains flakes 
and shreds of fibrin. 
The lungs are pressed backward and 
the adjacent organs are displaced. 

c. Purulent Pleuritis, Empyema, Pyo- 
thorax, results from micro-organ- 
ismal infection. It may begin as such, 
or as a primary serofibrinous pleu- 
risy, with secondary infection from 
various sources. The contents of the 
pleura may rupture into the lung or 
bronchi and sometimes through the 
chest wall. 

A rare termination is absorption of 
the pus or gradual inspissation, re- 
maining as cheesy detritus, which 
may become calcareous. 

d. Hemorrhagic Pleurisy generally re- 
sults from tuberculous infection or 
malignant disease of lungs or pleura. 
It may also result in old and cachec- 
tic individuals or in those suffering 
from scurvy, purpura, etc. 

The liquid varies from a light bloody 
serum to nearly pure blood. 

e. Chronic Pleurisy. This term may be 
used in cases of thickening of the 
pleural membrane following the vari- 
ous forms, but strictly, when the 
thickening is of a progressive pro- 
ductive character. In both cases the 
pleura is thickened by fibrous over- 
growth, which may be uniform or 
localized, or in the form of adhe- 
sions. 

. Infectious diseases. Tuberculosis and 
syphilis. 

. Tumors are rare. Fibromata, lipomata., 
chondromata, osteomata, primary 
and secondary sarcomata and second- 
ary carcinomata. 

. Parasites. Echinococcus cysts, amoe- 
bacoli. 



DISEASES OF THE DIGESTIVE 
SYSTEM. 

DISEASES OF THE MOUTH. 
1. Stomatitis or Inflammation. 

a. Catarrhal Stomatitis is caused by 
irritants, — chemical, physical, me- 



176 PATHOLOGY. 

chanical or bacterial, or some cases 
of lowered vitality. 

The mucous membrane of the mouth 
is at first red, dry and hot; later 
there is considerable liquid exuda- 
tion. Teeth impressions are found 
on the tongue, lips and cheeks, the 
gums are swollen and painful. If 
the condition is intense, cysts due 
to distended mucous glands and ero- 
sions may appear. If it is long con- 
tinued, white slightly elevated spots 
may be seen, which result from 
epithelial hyperplasia (leukoplakia). 
In gastro-intestinal and other dis- 
eases epithelial disquamation is ac- 
tive with retention of the cells on 
the surface, which, mixed with food, 
bacteria, etc., causes the "furring of 
the tongue." 

Localized disquamation gives rise to 
the so-called "geographical tongue." 

b. Apthous Stomatitis is seen in chil- 
dren and is due to malhygiene, de- 
bility or gastro-intestinal and other 
diseases. It is a form of herpes. 
Small whitish spots on an inflamed 
base are found on the mucous mem- 
brane, especially of the lower lips 
and gums. 

They are usually descrete, but some- 
times confluent. The spots are com- 
posed of desquamated epithelium, 
with occasional fibrin. Ulceration is 
seldom seen. 

Pednar's Apthae are small ulcers 
seen at the lateral portions of the 
palate, sometimes on the soft palate, 
and are probably due to traumatism 
occurring in the act of sucking. 

c. Ulcerative Stomatitis. In children it 
is the result of malnutrition and lack 
of cleanliness of the mouth. Various 
micro-organisms normally found in 
the mouth under certain conditions 
aid in its production. Cachectic con- 
ditions, as scurvy, etc., mercury and 
other forms of poisoning, leads to 
extensive ulcerations. 

It may also be secondary to necrotic 
conditions of the bones or suppura- 
tive inflammation about the roots of 
the teeth. The gums are reddened 
.and soft with sometimes hemorrhagic 



STOMATITIS. 177 

infiltration and epithelial destruction, 
resulting in ulcers. 

Suppuration may occur and loosen 
or even dislodge the teeth. 

Pyorrhoea Alveolaris begins around 
the necks of the teeth and second- 
arily involves the gums, results from 
some constitutional disease allied to 
gout. 

The ligament of the tooth is inflamed 
and retraction and suppuration of 
the gums follows. 

d. Pseudomembranous Stomatitis is 

usually secondary to pharyngeal 
diphtheria. 

e. Phlegmonous Stomatitis is seen in 
the . lips and results from trauma- 
tism, with intense infection or sec- 
ondary condition after erysipelas or 
other cellular inflammations of the 
face. The lips and cheeks are swol- 
len and suppuration may occur with 
abscesses rupturing into the mouth. 
A chronic form of the deeper tissues 
of the lips may cause hypertrophy. 

f. Gangrenous Stomatitis, Noma, Can- 
crum oris, occurs in ill-nourished 
children. It affects the mucous mem- 
brane in the form of a sloughing 
ulcer, with inflammatory induration 
of the entire thickness of the cheek. 
The skin is at first dark red, bluish 
or greenish, followed by gangrene. 
It follows measles in about one-half 
of all cases. Putrefactive changes 
cause an almost intolerable fetor. In- 
tense septic infection and intoxica- 
tion attends. 

2. Infectious Diseases. 

Thrush, Mycotic Parasitic Stomatitis, 
Parasitic Stomatitis, generally affects 
poorly nourished and hand-fed chil- 
dren and is due to the oidium albi- 
cans. (See Parasitic Diseases). The 
mucous membrane is inflamed, white 
spots appear here and there due to 
a mixture of mycelial threads of the 
parasite and degenerated epithelial 
cells and other micro-organisms. 
Tuberculosis, Syphilis and Actinomy- 
cosis are also met with. t 
3. Tumors. Papillomatous growths, 

fibroma, lipoma, myxoma, chondroma, 



178 PATHOLOGY. 

lymphadenoma, carcinoma, hemangi- 
oma and lymphangioma. 
Cysts from obstruction of mucous 
glands. 

Ranule, is a cyst that is formed by 
dilatation of the gland ducts, as seen 
in the ducts of mucous, sublingual, sa- 
livary or submaxillary glands. 

DISEASES OF THE TONGUE. 

1. Acute Glositis, from irritation caused 
by burns, stings of insects, traumatism, 
"foot and mouth disease" and various 
micro-organisms. The tongue is red 
and enlarged. Superficial or deep ab- 
scesses are occasionally formed. 

2. Chronic Glositis, from repeated attacks 
of the acute, irritation from excessive 
use of tobacco and alcohol, injury from 
bad teeth, and it has occurred from 
myxodema and cretinism. The tongue 
is enlarged and ulcerated at the edges. 

3. Macroglossia (muscular hypertrophy) 
may be unilateral or bilateral and due 
to lymphangioma. 

4. Atrophy and Degeneration from nerv- 
ous diseases. 

5. Infectious Diseases, as tuberculosis, 
syphilis and actinomycosis. 

6. Tumors. Same as in mouth. 

DISEASES OF THE SALIVARY 
GLANDS. 

1. Salivation, or Hypersecretion, is due 

to nervous disturbances, diseases as 
hydrophobia and smallpox, etc., cer- 
tain drugs and metals, pregnancy and 
some uterine disease. 
True idiopathic salivation is rare. 

2. Xerostoma, or dry mouth, is due to 

arrest of flow from the salivary or 
buccal glands. The mucous membrane 
is dry and slimy. The tongue is dry 
and red. It is caused by some nerv- 
ous influence. 

3. Inflammation. 

a. Parotitis may be an independent in- 
fection mumps or secondary to 
various infections, as typhoid fever, 
typhus fever or pyemia. 
In mumps the gland is swollen and 
tensely distends the capsule. The 



THE TEETH. 179 

exudate is serous and is removed by 
absorption. 

Secondary infection of the gland 
tends to abscess formation. Chronic 
induration may remain. 
b. Angina Ludovici, or Ludvigs Angina, 
is a septic inflammation, usually of 
the submaxillary arid adjacent parts. 
It results from streptococcic infection 
in the course of various diseases, 
principally scarlet fever. It may re- 
sult from a carious process at the 
roots of the teeth. It terminates by ab- 
scess formation with perforation. 
Necrosis or gangrene may result. 

4. Tumors. Sarcoma, chondroma, fibroma, 
myxoma, lipoma, concretions and 
cystic dilatations of the ducts 
(Ranula) and salivary fistula results 
from trauma or abscess. 

TEETH. 

1. Anomalous Development, absence, in 
size, number, delay in eruption, irregu- 
larity in formation and maldevelop- 
men£, as in case of congenital syphilis 
(Hutchinson's teeth), which are wedge- 
shape, the cutting edge is smaller than 
crown, and has a concave notch. These 
teeth are not entirely peculiar to 
syphilis. 

2. Caries of Teeth is due to malnutri- 
tion, digestive disturbance and un- 
cleanliness. 

Micro-organisms, leading to acid fer- 
mentation, soften the enamel and oc- 
casion fissures, which give entrance to 
other bacteria. There is gradual dis- 
integration of the enamel and dentine, 
with formation of granular detritus, in 
which are numerous bacteria. The 
process penetrates to the pulp and sec- 
ondary inflammation or pulpitis is set 
up. 

Caries may sometimes begin from 
within. 

3. Inflammation of Pulp is associated 
with caries or independently. The pulp 
is red, swollen, hemorrhagic, with later 
suppuration. The process spreads 
through the roots of the teeth to the 
alveolar periosteum, with sometimes ab- 
scess formation about the teeth. This 
may spread to the gums (alveolar ab- 



180 PATHOLOGY. 

scess) and rupture on the surface. 
4. Tumors. Odontomata resemble den- 
tine and arise from the pulp during de- 
velopment. They form irregular out- 
growths of the crown or root. Odon- 
tonoids are smaller outgrowths, resem- 
bling enamel, dentine or the cement 
substance, and are seen in later life. 
Sarcomata and fibromata arise from 
the pulp during development, or from 
the connective tissue around the root. 
Polypoid outgrowths are hypertrophied 
granulations. 

Giant-celled sarcoma, known as epulis, 
spring from the alveolar process of the 
jaw. 

Cysts arise from the primary follicles 
in which teeth are developed. 

DISEASES OF THE PHARYNX AND 
TONSILS. 

Inflammations of the Pharynx. 

1. Catarrhal Pharyngitis, or Angina, or 
Sore Throat, is due to irritations, as 
hot liquids, chemicals, exposure to 
cold and infections. It may affect the 
entire pharynx or be limited to the 
tonsils. The mucous membrane is 
bright red and sometimes swollen, with 
a tenacious exudate composed of mu- 
cous and desquamated cells. There 
may be vesicular elevations, which 
sometimes rupture and form super- 
ficial ulcers. There may be extravasa- 
tions of hemorrhage. 

Herpes angina is like herpes of the 
skin. 

2. Chronic Catarrhal Pharyngitis results 
from repeated attacks of the acute or 
excessive use of the voice, smoking and 
alcohol. The mucous membrane is at 
first swollen, but later it becomes 
atrophic, with hyperplastic lymph fol- 
licles or distended mucous glands ap- 
pearing as slight granular elevations. 
The submucous veins are enlarged and 
tortuous. 

3. Phlegmonon Pharyngitis is due to 

wounds or is associated with infections, 
as pseudo-membraneous tonsilitis and 
pharyngitis, smallpox, pustules of 
pharynx or pharyngeal glands. The 
soft palate, uvula and arches are swol- 
len and distended. There may be deep 



THE TONSILS. 181 

cyanosis and edematous exudation. 
Suppuration generally follows and 
sometimes gangrenous necrosis. There 
is often general septicemia. 
Retropharyngeal Abscess is secondary 
to trauma or infectious pharyngitis. 
Occasionally it is produced by caries 
of the vertebrae, embolism during some 
infectious fevers, or the infective germ 
may enter the lymph stream through 
the tonsils. 

4. Pseudo-membranous Pharyngitis is 

caused by the bacillus diphtheria or to 
various other organisms or irritations 
from gases or steam, etc. 
If non-diphtheretic it is common with 
scarlet fever, measles and other infec- 
tions, and seems to be due to the 
streptococcus. The throat appears like 
that of diphtheria, but extensive ne- 
crosis is more common. The mucous 
membrane and other parts, especially 
the tonsils, are swollen and edematous, 
with later necrotic changes. 

White or yellowish patch or patches 
appear in the throat, which coalesce as 
a rule and extend over the tonsil, 
fauces and uvula, or to the mouth, nose 
and larynx. The pseudo-membrane is 
firmly attached. 

Microscopically, the deposit is made 
up of meshes of fibrin containing de- 
generated leucocytes and epithelial 
cells, bacteria, etc. The deep tissues 
are intensely congested with round cell 
infiltration. The adjacent lymph glands 
are enlarged and may suppurate with 
sometimes extensive cellulitis and sup- 
puration of the floor of mouth. 

Inflammation of the Tonsils or Tonsilitis 

may occur associated with tonsilitis or 
may be independent. 

1. Catarrhal Tonsilitis is similar to ca- 
tarrhal pharyngitis. 

2. Follicular Tonsilitis, Lacunar or Croup- 
ous Tonsilitis involves the normal or 
chronic hypertrophied tonsils, and is 
due to causes similar to pharyngitis. 
White or yellowish spots appear, which 
are the lacunar or crepts distended 
with degenerated epithelial cells and 
bacteria, as staphylococci, streptococci, 
pneumococci, tubercle bacilli, diph- 



182 PATHOLOGY. 

theria bacilli, etc.; all play a part in 
the etiology. 

Ulceration may occur. The contents of 
the lacunae are discharged, or adhere 
like pseudo-membranes, or remain in- 
spissated and even calcify. 
Bacteria may penetrate the tonsil and 
cause, — 

3. Phlegmonous Tonsilitis, Abscess of the 
Tonsil, Quinsy, is due to an infection. 
It may result from the catarrhal or fol- 
licular, or may be associated with the 
phlegmonous inflammation of the 
pharynx. One or both tonsils may be 
affected. The tonsil is greatly swollen, 
red and its parenchyma is infiltrated 
with leucocytes and serum. Pus may 
form in the tonsillar or peritonsillar 
tissue. Rupture of the abscess may 
take place into the pharynx, or it may 
open on the neck at the angle of the 
jaw, or it may extend down the neck 
into the mediastinum. The internal 
caroted artery may be perforated. The 
submaxillary and cervical lymph glands 
are enlarged. There is frequently mild 
septicemia, myocarditis and nephritis 
may result. There appears to be a 
close connection between rheumatism 
and quinsy. 

4. Hypertrophy of the Tonsil results from 
repeated attacks of the catarrhal or 
follicular tonsilitis. The tonsils are 
irregularly enlarged and harder than 
normal. The connective tissue is in- 
creased and the lymphoid follicles are 
hyperplastic. Pressure upon the orifices 
of the crypts may obstruct and cause 
lacunar tonsilitis. The contents of the 
crypts are prone to be retained and 
calcified where the tonsils are hyper- 
trophied. 

Hypertrophied tonsils are frequent in 
badly nourished children and is asso- 
ciated with hvnerplasia of lingual ton- 
sil and adenoids of the nasopharynx. 

Infectious Diseases of the Pharynx and 
Tonsils. 

Diphtheria (see Bacterial Diseases), 
tuberculosis, syphilis, glanders, lepra, 
typhoid ulcers and pharyngomycosis 
leptothricia (leptothrix buccalis). 
Tumors. Polypoid tumors, hyperplastic 
adenoid growths, fibroma, lipoma, chon- 



ESOPHAGUS. 183 

droma, papilloma, sarcoma and epithe- 
loma. 

DISEASES OF THE ESOPHAGUS. 

1. Congenital Defects. The esophagus 
may be divided by a septum, or it may 
be absent altogether. It may open 
into trachea, or it may open onto the 
external surface of the neck. 

2. Circulatory Disturbances. Anemia, 
active hyperemia and passtive conges- 
tion. 

3. Inflammations. 

a. Catarrhal Esophagitis. There is hy- 
peremia and desquamation of epithe- 
lium and scant liquid secretion, 
caused by trauma, swallowing acid, 
alkaline or hot liquids. 

b. Chronic Catarrhal Esophagitis from 
long-continued passive congestion 
and alcoholism. 

c. Pseudo-membranous Esophagitis, 
diphtheria or pseudo-membranous 
pharyngitis. 

d. Ulcerative Esophagitis from pustules 
of smallpox, irritation of foreign 
bodies. Small or large ulcers may be 
present. Peptic ulcers may be found 
in the lower end. 

4. Stenosis is due to pressure of tumors 
or aneurysms, lodgment of foreign 
bodies, tumors of esophageal walls or 
stricture following ulcers, etc. 

5. Dilatation. 

a. Simple Dilatation or Ectasia, is gen- 
erally seen at the lower end and is 
due to obstructions at the cardiac 
end of the stomach. 

b. Diverticula. 

1. Pulsion Diverticula is generally 
situated at the upper portion of 
the esophagus and is due to pres- 
sure from within, the muscular 
coat being thinned. 

2. Traction Diverticula are generally 
situated at the lower end of eso- 
phagus and are due to adhesions 
of diseased bronchial glands and 
subsequent contraction. Perfora- 
tion may occur with septic infec- 
tion of pleura, pericardium and 



184 PATHOLOGY. 

lungs. Large arteries may be per- 
forated. 

6. Perforation and Rupture from necrotic 
or suppurative processes of the eso- 
phagus or adjacent structures, aneu- 
rysms of thoracic aorta, etc. 

7. Infectious Diseases. Tuberculosis 
(rare), syphilis, typhoid ulcerations, 
thrush. 

8. Tumors. Fibroma, myoma, lipoma and 
sarcoma are rare. Papilloma and car- 
cinoma. 

DISEASES OF THE STOMACH. 

1. Congenital Defects. Atresia of pylorus, 
division by septa, hour glass contrac- 
tion and sometimes absence. 

2. Circulatory Disturbance. 

a. Anemia, as part of general anemia. 

b. Hyperemia. 

1. Active. Functional during diges- 
tion. Inflammations and irritating 
agents. Punctate hemorrhages may 
occur. 

2. Passive. Heart disease and ob- 
struction to portal circulation. Mi- 
nute hemorrhages may occur. When 
congestion has existed for some 
time dark or bluish punctate pig- 
mentation occurs and chronic gas- 
tritis results. The changes are 
more marked near the pyloric end. 

c. Hemorrhage. Small hemorrhages 
may occur from active and passive 
congestion, inflammation, infectious 
or hemorrhagic diseases. Large 
hemorrhages occur from congestion 
in cardiac disease or cirrhosis of 
the liver, gastric ulceration or car- 
cinoma. The vomit of blood which 
is in a semi-digested condition 
(coffee ground vomit) is significant 
of carcinoma. 

Melaena Neonatorum. The blood 
vomit of the new born is due to 
gastric hemorrhages of disturbed 
circulation in insufficient respira- 
tion and possibly infectious hem- 
orrhage diseases. 

3. Inflammation. 

a. Acute Gastritis, Acute Inflammation 
of the Mucosa, is due to chemical, 



STOMACH. 185 

mechanical or thermal irritations and 
sometimes to infection. The mucous 
membrane is red, swollen and cov- 
ered with mucous. The gastric se- 
cretion is reduced and the mucous 
and peptic cells are granular and 
swollen. The inter-tubular tissue is 
infiltrated with round cells. The 
lymphatic tissue of the mucosa is 
hyperplastic. The seat is more fre- 
quently near the pyloric end. 

b. Pseudo-membranous Gastritis is due 
to corrosive poisons, smallpox, ty- 
phoid fever and septicemia, diph- 
theria, etc. There is an irregular 
pseudo-membrane, with sometimes 
necrosis and ulceration. 

c. Ulcerative Gastritis, from extreme 
congestion and acute gastritis, 
pseudo-membranous gastritis, septic 
embolism, and rarely infectious ul- 
ceration from tuberculosis, anthrax 
and typhoid fever. 

d. Chronic Gastritis. 

Causes. Repeated attacks of the 
acute, errors in diet, abuse of al- 
cohol, tobacco, anemia, gout, tuber- 
culosis, diabetes, albuminuria, ulcer, 
dilatation, chronic heart disease and 
cirrhosis of the liver. 
Pathologic Anatomy. The mucous sur- 
face is rough and wrinkled. Mucosa 
is of a grayish color, the veins are 
enlarged and there may be ecchy- 
mosis or small hemorrhages. There 
is cloudy swelling or atrophy of the 
gland cells so that the different cells 
can not be recognized. The glands 
may be obliterated, inflammatory 
processes press upon and destroy the 
tubules, bringing on a condition of 
sclerosis of the mucosa and sub- 
mucosa. The stomach walls may be 
thin and the stomach itself dilated, 
or the wall may be thickened and 
the stomach actually reduced in size. 

There is occasionally complete 
atrophy of the secreting tissue, the 
mucosa is then smooth, with occa- 
sional erosion of its surface. 

Pathologic Physiology of Gastritis. All 

forms of gastritis disturb the func- 
tions of the stomach, giving rise to 
the terms indigestion and dyspepsia, 



186 PATHOLOGY. 

due to abnormal secretion of the gas- 
tric glands, reduced motor power of 
walls and altered nervous mechan- 
ism. 

In some instances the amount of hy- 
drochloric acid remains normal, in 
others there is absence of acid and 
then again both acid and ferments 
are lacking. 

The general metabolism suffers and 
emaciation and systemic depression 
follows. 

Toxic substances produced in the 
stomach may contribute to the meta- 
bolic disturbances. 
4. Gastric Ulcer, Peptic or Round Ulcer. 

About 60% of cases occur in females, 

and young women seem particularly 

liable. 

Causes. Anemia and general malnutri- 
tion. The ulcers are due to the ac- 
tion of the gastric juice upon the 
parts of lowered vitality, and in- 
creased acidity is probably an impor- 
tant factor. 

Areas of lowered vitality may be due 
to embolism or thrombosis with in- 
farction. Spasms of the blood vessels 
and thickening of the vessel walls, 
trauma, etc. 

Pathologic Anatomy. The number of 
ulcers present varies, but generally 
there is only one. The situation is, 
as a rule, in the lesser curvature 
on the posterior wall near the pyloric 
end. They may, however, be found 
at the fundus or at the cardiac end. 
They vary in size from a few m m. 
to 5 cm., and have sloping edges 
(funnel form), with the apex toward 
the muscular coat. The edges are 
irregular and rough, but may be 
smooth and rounded. 
Ulcers may cause perforation, fatal 
hemorrhages, deformity by contrac- 
tion and loss of much secreting 
structure. 

In the healing of ulcers scars are 
formed, which have usually a char- 
acteristic stellate shape. 
If the ulcers are large, extensive con- 
traction results. Hour-glass contrac- 
tion of the stomach or pyloric sten- 
osis may occur, with resulting sec- 
ondary conditions, as dilatations, etc. 
4. Atrophy is caused by senility, chronic 



STOMACH. 187 

gastritis, chronic diseases, as pernicious 
anemia, etc., gastric dilatation and 
contraction of cardiac orifice of stom- 
ach. 

5. Degenerations. Fatty degeneration, 
pigmentation, amyloid degeneration, 
calcification and gastro-malacia (sim- 
ple softening of walls) is usually a 
post mortem condition. 

6. Alterations in Position and Size. The 
stomach may be displaced into the 
thoracic cavity through rupture of the 
diaphragm (diaphragmatic hernia); 
through the abdominal walls when 
these are congenitally deficient, and 
downward (gastroptosis) from dilata- 
tion, adhesions, tight lacing, enlarge- 
ment of spleen or relaxed abdominal 
walls. 

Dilatation or Gastrectasia. 
Causes. Cicatricial contraction at py- 
lorus; cancer at or near the pylorus; 
fibroid hypertrophy and contraction 
at the pyloric end from gastritis, 
pressure of an aneurysm, movable 
kidney or tumor. A dilatation of 
stomach called atonic dilatation may 
be caused by over-eating, excessive 
beer drinking v> chronic gastric ca- 
tarrh, exhausting diseases and gen- 
eral muscular debility. It is due to 
weakening of the stomach walls. It 
may also be caused by abnormal ad- 
hesions of the stomach. 
Pyloric stenosis may at first be com- 
pensated for by hypertrophy of the 
muscles of the stomach, then the 
stomach dilates, food stagnates and 
ferments (Sarcinae ventriculae are 
often present and lactic, butryic and 
acetic acids, sulphuretted hydrogen 
may result) and dilatation is in- 
creased. The mucosa is thin and oft- 
en degenerated and atrophic. 

7. Infectious Diseases. Tuberculosis ul- 
cerations, syphilic gummata or ulcera- 
tion may occur, anthrax and thrush. 

8. Tumors. 

Connective tissue tumors. Fibroma, 
myoma, lipoma, may be seen and 
sarcoma is rare. 

Epithelial tumors. 

a. Polypoid elevations and adenoma- 
tous proliferations. 



188 PATHOLOGY. 

to 

b. Carcinoma is a frequent tumor of 
the stomach. Hard or scirrhous, soft 
or medullary, adenocarcinomata or 
adenoma, cylindrical-celled and squa- 
mous-called carcinoma. 

The cancers are most frequently sit- 
uated at or near the pylorus. Stag- 
nation of food and fermentation re- 
sults. Hcl is absent. Lactic acid 
secretion is pronounced. Stomach di- 
lates. A long thread-like bacillus 
(Oppler-Boas) is present and is sup- 
posed, by a few, to occur only in 
cancer of the stomach. Metabolism 
is disturbed, etc. 

DISEASES OF THE INTESTINES. 

1. Congenital and Acquired Abnormali- 
ties. 

a. Total absence has been seen in mon- 
strosities. 

b. Narrowing or distortion is more fre- 
quent. 

c. There may be congenital enlarge- 
ments of the intestines and localized 
dilatations, notably Merckle's diver- 
ticulum, which represents the re- 
mains of omphalomesenteric duct. 
This may be open at the umbilicus 
and diverticula may be formed as a 
result of constipation or localized 
weakening of the muscular walls, al- 
lowing a protrusion of the mucosa. 

d. There may be congenital abnormali- 
ties of position, e. g., ascending color, 
and cecum, situated on the right side, 
etc. 

e. Enterocystoma is a congenital 
cystic condition sometimes seen a; 
the umbilicus from cystic dilatation 
of parts of omphalomesenteric sys- 
tem of the foetus. 

f. Narrowing or stenosis may be seen 
and is due to pressure of tumors or 
displaced viscera, cicatricial constric- 
tions from ulcerations or to neo- 
plasms. 

Narrowing of the lumen may be due 
to carcinoma or tumors within. 

g. Hernia is a displacement of any of 
the viscera from the cavity in which 
it normally lies. 



INTESTINES. 1SH 

Causes. 

1. Congenital, occasionally. 

2. Acquired. A weakness of the ab- 
dominal wall and abnormal mova- 
bility of the intestine acts as a pre- 
disposing cause, while a strain acts 
as an exciting cause. 

Varieties. 

Internal Hernia is displacement of vis- 
cera into other cavities within the 
body, as into the thorax diaphrag- 
matic hernia; into retroperitoneal 
space (retroperitoneal hernia). 

External Hernia is a displacement of 
the viscera through the abdominal 
wall and may be divided into: — 

1. Inguinal Hernia. Protrusion 
through external inguinal ring. The 
intestine descends through the in- 
guinal canal sometimes as far as 
scrotum (indirect inguinal heria), 
or protrusion takes place directly 
through the internal inguinal ring 
and may present itself under the 
skin or descend through the lower 
part of inguinal canal into scrotum 
(direct inguinal heria). 

2. Femoral Hernia is frequently seen 
in women. The intestine pushes 
through the femoral ring and pre- 
sents itself on the inner side of 
the thigh at the saphenous open- 
ing. 

Other varieties are, — ventral, vag- 
inal, rectal, perineal, ischiatic or 
obturator, 

Hernia consists of a sac (perito- 
neum) and its contents, which is 
intestines or portions of omentum 
or both. Secondary changes, as 
inflammations of the sac and in- 
testines, which may lead to fibrous 
adhesions, contracting the sac and 
binding the intestines in place. 
Hernia may be divided into, — 
Reducible, or irreducible, in accord- 
ance to ability of replacing con- 
tents into peritoneal cavity or not. 
If there is pressure at the neck of 
the sac by inflammatory exudation 
or constrictions or accumulations 
within the bowel so as to obstruct 
the circulation of the intestinal 



190 PATHOLOGY. 

hernia. Intense passive congestion 
and inflammation of the peritoneal 
coat follows and gangrenous ne- 
crosis frequently results. This is 
called Strangulated hernia. 

2. Intestinal Obstruction. 

a. Internal Strangulation by peritoneal 
adhesions or the intestine slipping 
through openings or perforations of 
the mesentery or omentum. 

This causes great dilatation of the 
intestine above the obstruction and 
collapse of the intestine below. 
Congestion and peritonitis, necrosis 
and perforation may occur at the 
point of stricture. 

b. Volvulus is a twist of some part of 
the intestinal canal and due to ab- 
normal laxity of the mesentery, 
which predisposes, and general strain 
or abdominal compression acts as the 
exciting cause. 

The vessels may become obstructed 
and hemorrhagic infarction is often 
seen. Gangrene of bowel may re- 
sult. 

c. Intussusception, or Invagination, is a 

slipping of one part of intestine into 
an adjoining part. The upper part 
of the intestine is induplicated and 
pushed into the lower part. It is 
due to irregular peristalsis from 
atony of one part with increased ac- 
tivity of another part. Polypoid 
tumors within the bowel are dragged 
by peristalsis from the upper part of 
bowel into the lower part. It is more 
common in children than in adults. 
The invagination most frequently 
takes place in the iliocecal region. 
The serous surfaces tend to unite by 
peritonitis, and the invagination por- 
tion may become gangrenous and be 
discharged, which may result in re- 
covery. Otherwise perforation pro- 
duces fatal peritonitis. 

d. Prolapse of Rectum is due to weak- 
ness of the sphincter and other parts 
of the wall with straining. It is fre- 
quently seen in infants and some- 
times in adults. It may be occa- 
sional or constant. • 

Secondary inflammation, ulceration 



INTESTINES. 191 

and even necrosis may result. 

3. Circulatory Disturbances. 

Active and passive hyperemia, hemor- 
rhage, edema, embolism and thrombosis 
are often seen. 

Hemorrhoids result from varicose veins 
of the rectum and are generally 
found in or outside of the sphincter 
muscle, and are designated as inter- 
nal or external hemorrhoids. They are 
due to obstruction to the venous cir- 
culation from cirrhosis of the liver, 
repeated pregnancies, pelvic tumors or 
chronic constipation. 

The hemorrhoid presents itself as a 
congested small polypoid elevation, 
consisting of slightly or greatly di- 
lated veins, between which is a more 
or less amount of inflammatory con- 
nective tissue. Thrombosis within the 
cavities often occurs. Infection of the 
veins may occur and hemorrhoid en- 
larges and becomes inflamed and ede- 
matous. 

4. Inflammation. 

Enteritis, or Inflammation of the Intes- 
tines, involves particularly the mucosa 
and submucosa of any part of the 
gastro-intestinal tract, and is most fre- 
quent in children and the aged. 

Causes. Irritating foods; poisons of 
various kinds; poisons produced by 
improper digestion and fermentation; 
bacteria, of which the normal colon 
bacillus plays an important part, in 
that it increases in violence under cer- 
tain conditions, but other organisms 
undoubtedly play an important part. 

Pathologic Anatomy. 

a. Catarrhal Enteritis. The mucosa is 
swollen and of a light red color. The 
arteries are distended and sometimes 
there may be petechial hemorrhages. 
On the surface there is a mucous 
exudate containing desquamated and 
degenerated epithelial cells and emi- 
grated leucocytes. The contents of 
the intestine is liquid by serous exu- 
dation. 

The solitary or agminated follicles 
are enlarged and the term follicular 
enteritis is given. 



192 PATHOLOGY. 

The desquamation of the epithelium 
may be more marked than the mu- 
cous exudation, shreds of mucous 
may be discharged and the term 
croupous enteritis is given this form. 

b. Suppurative Enteritis differs from 
the above, in that there is a greater 
emigration of leucocytes in the exu- 
date, and in intense cases the sur- 
face may be covered with pus. The 
mucosa and submucosa show round 
cell infiltration and submucous ab- 
scesses, or ulcers are sometimes 
seen. The solitary follicles tend to 
break down and form follicular ulcers. 

c. Pseudo-membranous Enteritis in- 
volves the large intestine and is es- 
pecially seen in dysentery. Diph- 
theria with pseudo-membranous de- 
posits may occur. 

d. Chronic Enteritis is due to repeated 
attacks of the acute, chronic conges- 
tion, tuberculosis, dysentery and er- 
rors in diet. The pathologic changes 
are in some cases identical with those 
of the acute form. In others the 
changes are more pronounced, ulcera- 
tion, pigmentation from hyperemia 
and blood extravasation, thickening 
and induration from proliferative 
connective tissue changes in the 
glandular tissue, or thinning and 
wasting of the villi and follicles and 
contraction from healing ulcers. 

In the later stages atrophy may en- 
sue, which may affect the mucosa 
alone, but often involves the muscu- 
laris also. 

Pathologic Physiology. 

General systemic intoxication may 
result from absorption of bacterial 
products, may produce depression or 
shock by local irritation acting 
through the nervous system. 

Exudation into the intestine may de- 
plete the vascular system and cause 
failure of the circulation. 

Peristaltic movements may be ar- 
rested and constipation results, 
though peristalsis is generally in- 
creased and enormous exudation 
produces diarrhoea. Digestion fails 
from the disease of the bowel and 



APPENDICITIS. 193 

premature expulsion of the intestinal 
contents. 

Marked disturbance of health re- 
sults. 
Duodenitis is associated with gastritis 
and is prone to obstruct the bile duct 
by inflammatory thickening and the 
accumulation of mucous at the 
mouth of the duct, and by this ob- 
struction gives rise to catarrhal 
jaundice. 

Inflammation of the Ileum is of the 

same character as enteritis, with 
conspicuous follicular form. It is 
common in children suffering from 
infectious fevers, as scarlet fever and 
diphtheria. The Pyers patches are 
enlarged and sometimes ulcerated 

Typhilitis or cecitis inflammation of 
the cecum. It is of the simple ca- 
tarrhal variety and is due to irrita- 
tion produced by constipation (ster- 
coral typhilitis). 

If the constipation is severe or ob- 
struction takes place ulceration may 
occur. 

Appendicitis may be a primary condi- 
tion or it may be due to direct ex- 
tension of typhilitis; or the thicken- 
ing of the mucosa and the accumu- 
lation of mucous in consequence of 
the typhilitis, which may cause ob- 
struction of the appendix. The re- 
tained appendiceal contents, together 
with the increased action of bac- 
teria, such as the colon bacillus, 
streptococcus, staphylococcus, etc., 
produces distention and congestion, 
the bacteria penetrate the mucosa 
and appendicitis results. In cases 
where fecal concretions and foreign 
bodies are found within the appen- 
dix they may be considered not as a 
direct cause, but by their irritation or 
injury to the mucosa the entrance of 
bacteria is rendered more easy. It 
may also be considered that the con- 
cretions found within the appendix 
have been formed from mucous or 
desquamated epithelial cells after the 
disease has begun. The part which 
the obstruction of the appendiceal 
arterial supply plays in the etiology 
of the disease is probably secondary. 



194 PATHOLOGY. 

Pathologic Anatomy. 

a. Catarrhal Appendicitis. The mu- 
cosa is slightly swollen and eroded, 
the muscularis and serosa may be 
congested and edematous, the appen- 
diceal contents is retained and is 
more or less muco-purulent. 

b. Necrotic or Gangrenous Appendi- 
citis. The mucosa is rapidly de- 
stroyed with extension of the process 
into the muscularis and serosa, and 
results in a local fibrinous peritoni- 
tis, which serves to retard the in- 
fective process and prevents diffuse 
peritonitis. If gangrene is very rapid 
with early rupture of appendix and 
escape of abundant bacteria, general 
peritonitis results before a wall can 
be formed. 

c. Interstitial Appendicitis. There is 
more or less of a productive connec- 
tive tissue change in all cases of ap- 
pendicitis, but in this particular form 
the change is particularly conspicu- 
ous in all the coats and frequently 
terminates in chronic thickening of 
the appendix. 

Colitis is generally due to irritation by 
fecal accumulation. The sigmoid 
flexure is the common seat. 
There is a thickening of the mu- 
cous membrane and abundant mu- 
cous exudation, later there is atrophy 
and sometimes ulceration. Masses of 
mucous or casts of the bowel may be 
discharged (Mucous colitis). 

Proctitis, or Inflammation of the Rec- 
tum, is due to irritation of fecal 
matter, parasites, etc., tumors, hem- 
orrhoids, etc. It may be a part of a 
colitis with like conditions. Ulcera- 
tive processes may extend to sur- 
rounding tissues and cause abscesses 
with a fistulous communication with 
the rectum or exterior. 
5. Infectious Diseases. 

a. Dysentery is a specific inflammation 
of the large intestine. It may be 
endemic or epidemic. 

Causes. In mild cases tainted foods 
and products of fermentation, with 
probably specific bacteria, poisons 
like mercury, etc., may cause it. 



CHOLERA. 195 

In the ulcerative form of the tropics, 
the amoeba coli is considered the 
cause. 

Pathologic Anatomy. 

1. Catarrhal Dysentery. There is 
congestion, swelling and edema of 
the mucous membrane, petechial 
hemorrhages and follicular en- 
largements or ulcers are met with. 

2. Ulcerative Dysentery. The mu- 
cosa is very much swollen by a 
serous or sero-hemorrhagic infil- 
tration and covered with a sticky 
mucous or muco-purulent exudate. 
The ulcers become chronic and in- 
dolent. There is great thickening 
of the bowel. 

3. Diphtheretic Dysentery. A pseudo- 
membrane of a grayish or brown- 
ish character appears on the mu- 
cosa. It is more or less necrotic 
and covers the entire wall of the 
colon or rectum, or is scattered in 
small areas here and there upon a 
thickened catarrhal surface. In 
mild cases the membrane is super- 
ficial; in severe cases it may ex- 
tend into the submucosa, and if 
detached leaves an irregular ulcer, 
which later becomes dirty-gray or 
brownish in color. Gangrenous 
dysentery is applied to the most 
violent form. 

In all cases the bowel is thickened. 
Occasional perforation may occur 
with peritonitis, periproctitis, etc. 
Embolism or ascending thrombosis 
of the portal vein frequently causes 
liver abscess. 

b. Cholera. (See Bacterial Diseases). 
The mucosa is red and swollen, with 
frequent petechial ecchymosis. There 
is extensive degeneration of the 
epithelium, which is probably a co- 
agulation necrosis. The solitary fol- 
licles or Pyers patches are enlarged 
and sometimes ulcerate. There is a 
great quantity of serous exudation 
containing flakes of desquamated 
and degenerated epithelium, which 
gives rise to the "rice water" stools. 
In later stages pseudo- membranous 
inflammation may be met with, and 
probably results from secondary in- 



196 PATHOLOGY. 

fection. Lobular pneumonia is a fre- 
quent complication. 

c. Typhoid Fever. (See Bacterial Dis- 
eases). 

d. Syphilis is most frequently seen in 
the rectum, where it may appear in 
the form of warty elevations or as a 
chancre, mucous patches and gum- 
matous nodules or infiltrations. The 
mucosa and submucosa is thickened 
and ulcerated, secondary cicatriza- 
tion and stenosis (syphilitic stricture) 
results. 

It may also be seen in the small 
intestine and the colon in the form 
of localized or diffuse gummata, with 
sometimes ulceration, particularly in 
congenital syphilis. 

e. Anthrax and Actinomycosis. (See 
Bacterial Diseases). 

f. Enteromycosis results from ingestion 
of putrid meat, fish, sausages, etc. 
The lesions are similar to catarrhal 
enteritis or croupous or pseudo- 
membranous inflammation or erosion 
or ulceration. The acute general 
symptoms are probably produced by 
bacterial poisons in the foods rather 
than by the bacteria themselves. 

6. Tumors. 

Connective Tissue Tumors. Fibroma, 
myxoma and lipoma. Sarcoma is 
rare. 

Epithelial Tumors. Inflammatory pa- 
pilloma, adenoma and carcinoma. 

7. Parasites. Tubercle bacillus, glander 
bacillus, typhoid bacillus, streptothrix, 
actinomycosis, bacillus coli communis. 
Protozoa, as coccidial psorospermia, 
Lamblia intestinalis and amoeba dys- 
enteria. The Tania saginata and so- 
lium, Dibothriocephalus latus. Ascario 
lumbricoides, Ankylostomum duodenale. 
Oxyuris vermicularis and Trichinella 
spiralis. The larva of various flies, etc. 

Rupture of the Intestine may be due 

to traumatism or penetrating 
wounds, ulcerations, such as duo- 
denal (peptic), appendiceal, typhoid, 
tubercular, dysenteric ulcers, etc. 
Foreign bodies may be swallowed and 
lodge in the intestine. Fecal con- 



LIVER. 197 

cretions or enteroliths, which con- 
sist of a nucleus of epithelial cells, 
mucous, hairs and earthy salts. They 
may cause great irritation and even 
perforation. 

LIVER. 

1. Circulatory Disturbances. 

a. Anemia. As a part of general anemia, 
pressure on liver from disease of its 
substance or compression of blood 
vessels. 

b. Hyperemia. 

1. Active, — physiologic during diges- 
tion, and associated with inflamma- 
tory abdominal diseases. 

2. .Passive, — from obstruction to cir- 
culation of cardiac or pulmonary 
disease, pleural effusions or adhes- 
ions, thrombosis of inferior vena- 
cava. 

The liver is enlarged, edges are 
rounded and color is darker than 
normal. 

On section, the central veins are 
seen to be congested and surround- 
ed by lighter areas. If the process 
persists, secondary fatty degenera- 
tion or atrophy of peripheral zone 
takes place which gives rise to the 
term nut- meg liver. There may be 
small hemorrhages into the sub- 
stance beneath the capsule. If 
in the late stages degeneration and 
reduction in size takes place and 
the liver becomes dark red in color 
from deposit of blood pigment, the 
term red atrophy is given. 
If there is a hyperplasia of connec- 
tive tissue between the lobules and 
acini with pigmentation, the term 
cyanotic induration is given. 
The hepatic function is 1 disturbed 
and jaundice results from pressure 
on the biliary ducts and capillaries. 

c. Embolism and Thrombosis of the 
portal vein occurs in various diseases 
of the gastrointestinal tract particular 
ulcerative enteritis. 
2. Atrophy, senility, inanition and or- 
ganic diseases, pressure, etc. Portions 
of the liver or the greater part of its 
structure may be involved. The liver 



198 PATHOLOGY. 

is uneven and more or less pigmented. 
The liver cells are decreased in size 
and granular. The acini may disappear 
and hyperplasia of the stroma and pro- 
liferation of the biliary ducts may oc- 
cur. Acute yellow atrophy — see below. 
Red atrophy — see congestion. 

3. Degeneration. 

a. Pigmentation, Hemotogenous, biliary 
and rarely anthracotic pigmentation 
occurs. 

b. Fatty Infiltration, may be physiologic 
in children and overfed persons. 
Pathologically it occurs from the us- 
ual causes. 

c. Parenchymatous or cloudy swelling. 

d. Fatty degeneration, and 

e. Amayloid, in consequence of syphilis- 

f. Dropsical Infiltration, in intense in* 
fection and intoxication. 

g. Acute Yellow Atrophy, which is the 
most advanced fatty degeneration oc- 
curring in the liver. 

Causes. It is most frequently seen in 
young women, especially those who 
use alcohol in excess. Intoxications, 
by phosphorus, alcohol and bacteria. 
Syphilis seems to act as a cause 
and parturition acts as a determining 
cause. 

Pathologic Anatomy. The liver may 
at first be increased in size, but gen- 
erally it is decreased, soft and friable. 
On section it is of a brownish or 
grayish color (due to degenerated 
and pigmented hepatic cells) with 
bright red areas here and there (due 
to foci of hemorrhagic infiltration or 
pigmentation). 
• The hepatic cells undergo rapid fatty 
degenerations or necrosis and are re- 
placed by yellow pigment particles. 
It leads to intense cholemia. 

4. Inflammations or Hepatitis. 

a. Parenchymatous Hepatitis, is due to 
infections and intoxications. The liv- 
er cells undergo a certain amount of 
degeneration. 

b. Acute Intestitial Hepatitis or Liver 
Abscess, is due to microorganisms, as 
amoeba of dysentery, staphylococcus, 
streptococcus, bacillus coli communis, 



LIVER. 199 

etc., gaining access to the liver, di- 
rectly, by penetrating wounds or gas- 
tric or duodenal ulcers, etc., or in- 
directly through the circulation or by 
invasion along the bile ducts. 

It is probably brought about most 
frequently by ulcerations of the in- 
testine, particularly dysentery, the 
germ being carried to the liver 
through the circulation. 

In the tropics, traumatism without 
any apparent contusion may occasion 
abscess. It is probably due to micro- 
organisms entering the injured part 
from the biliary passages. 

Pathologic Anatomy. 

The traumatic or dysenteric abscess- 
es are solitary. They begin as small 
grayish or yellowish spots. Softening 
takes place and a cavity is formed 
which is filled with a creamy pus 
often having a reddish appearance. 
The cavity may increase to enormous 
proportions and may be partially ta- 
bulated. Multiple abscesses may 
sometimes be present. If the cavity 
is small, pus may be absorbed and a 
cicatrix may result, or pus may be 
inspissated and encapsulation may en- 
sue. Large abscesses may rupture 
into the stomach, intestines or the 
cavities. 

Metastatic abscesses or those due to 
extension of infection from the ducts 
etc., are multiple and of small size. 

c. Chronic Interstitial Hepatitis or 
Cirrhosis of the liver, is a diffuse 
hyperplasia of the interlobular con- 
nective tissue, sometimes extending 
into the acini or causes secondary 
changes in the liver cells. 
Causes. Alcohol and overeating con- 
tributes, syphilic, malaria or tuber- 
culosis. Some authorities have as- 
signed bacteria, entering the portal 
circulation from the intestines, as a 
cause. 

Pathologic Anatomy. 

1. Atrophic Cirrhosis ("Gin -drinker's 
liver") is the ordinary form. 
In the early stages the liver is 
often enlarged but later it is con- 
tracted, hard granular and irresru- 



200 PATHOLOGY. 

lar on the surface. Bands of dull 
gray or white connective tissue sur- 
round the yellowish or brownish 
acini and compress them so that 
they rise above the surface. 
Microscopically there is at first 
round cell infiltration and connec- 
tive tissue proliferation. The com- 
pression of the acini may cause 
them to denegerate. New formed 
biliary ducts may be present. 

The portal circulation is obstruct- 
ed and congestion of the spleen and 
gastro -intestinal mucosa with 

ascites follows. 

If the obstruction is extreme, col- 
lateral circulation may relieve the 
portal congestion. The communica- 
tion may be between the gastric and 
esophageal veins and between the 
hemorrhoedal veins and the veins of 
Retzius with the retroperitoneal 
veins. The veins of the round liga- 
ment may communicate with the 
veins at the umbilicus. Jaundice is 
rare, as the bile ducts are rarely 
compressed. 

Pathologic Physiology. Gastroin- 
testinal disturbances from obstruc- 
tion to the portal circulation, and 
metabolic disturbances. 

2. Hypertrophic Cirrhosis, is more of- 
ten seen in warm climates. 

The liver is uniformly enlarged, 
smooth and indurated. On section 
it is of a yellowish or greenish 
color. Interlobular proliferated con- 
nective tissue is present and ex- 
tends into the acini every where be- 
tween the columns of hepatic cells. 
Proliferated bile-ducts are seen 
within the new formed connective 
tissue. There is frequent prolifer- 
ation of the liver cells. 
Jaundice is prominent. Obstruction 
to the portal circulation is rarely 
marked. 

3. Biliary Cirrhosis, is consequent up- 
on obstruction of the biliary ducts. 
Toe liver is swollen from retention 
of the bile and is sometimes con- 
gested. Stagnation of the bile takes 
place and the irritating substances 
produced leads to reactive inflam- 
mation. The appearance of th« 



GALL, BLADDER. 201 

liver is much like that of the hy- 
pertrophic form. There is marked 
proliferation around the interlobu- 
lar biliary capillaries and multipli- 
cation of new bile ducts and hepatic 
cells may be seen from the first. 
If the gall ducts are absolutely ob- 
structed and active fermentative 
changes in the bile has occured. 
rapid fatty degeneration and acute 
atrophy of the liver results. 

Perihepatitis or Inflammation of the 
Capsule of the liver, may be an ex- 
pression of syphilitic infection or oc- 
cur alone or in association with 
peritoneal thickening. 

It may be associated with cirrhosis. 
The capsule is thickened and may 
cause atrophy of the underlying 
hepatic substance. 

5. Infectious Diseases. 

a. Tuberculosis, is always secondary 
and is of the miliary form. The 
tubercles arise in the interlobular tis- 
sue or from the acini. 

b. Syphilis, is seen as diffuse infiltra- 
tions and cirrhosis or in the form of 
gummata. It occasions overgrowth of 
connective tissue around parenchy- 
matous distruction which becomes 
necrosed with subsequent contraction. 
This causes the irregular tucking in 
of the liver surface, pathognomonic of 
syphilis. 

c. Leprosy is rare. 

6. Tumors. Fibromata, lipomata, myo- 
._ mata, angiomata, sarcomata (gener- 
ally secondary), lymphadenomata, ade- 
nomata, carcinomata (general second- 
ary), and cysts, — are rare. 

7. Parasites. Amoeba dysenteria, Psoros- 
permiae, Fasciola hepatica, Dicrocoelum 
lanceatum, Schistosomum haematobium. 
Ascarides and the Taenia echinococcus 
causing the echinococcus cysts (see 
Parasitic Diseases). 

BILIARY DUCTS AND GALL BLADDER. 

1. Inflammations, 
a. Cholangitis or inflammation of the 
biliary ducts, is due to duodenal ca- 
tarrh or irritation, of gall stones, 
foreign bodies from the intestine or 
parasites or bacteria. 



202 PATHOLOGY. 

The mucosa is swollen, edematous 
and secretes abundant mucous. The 
duct is obstructed with retention of 
bile and jaundice. 

b. Suppurative Cholangitis, may occur 
in consequence of infectious diseases, 
but generally from obstruction to the 
common or the hepatic duct. Bac- 
terial invasion and sometimes from 
rupture of liver abscess into the bile 
ducts may cause it. The pyogenic 
micrococci and Bacillus Coli com- 
munis are frequently found in sup- 
purative cholangitis. 

The ducts are filled with decomposed 
bile or a puriform liquid and the 
large ducts, especially, present an 
ulcerated or necrotic appearance. 

c. Chronic cholangitis, may follow an 
intense attack of the acute, but gen- 
erally it is due to chronic obstruc- 
tion of the ducts and retention of the 
bile. 

Intense inflammatory lesions follow- 
ing the passage of stones may cause a 
cicatricial stenosis. 

d. Cholecystitis or inflammation of the 
gall bladder, results from an extens- 
ion of cholangitis or the irritation of 
retained bile or gall stones. It is 
common in typhoid fever and the 
Bacillus typhosis may be found in 
the contents of the gall bladder. The 
wall is thickened, mucous membrane 
is swollen and ulcerated. The gall 
bladder may be filled with pus 
(empyema of the gall bladder). Rup- 
ture may take place into the periton- 
eal cavity, viscera or externally. 

2. Stenasis of the ducts, result from acute 
inflammations, chronic cholangitis with 
cicatricial overgrowth of connective 
tissue, impaction of gall stones or for- 
eign bodies, pressure of aneurysms or 
tumors, adhesions from peritonitis, all 
lead to retention of bile and dilation 
of ducts above, with consequent en- 
largement of the liver and jaundice. 

Obstruction to cystic duct, generally 
from stone, may occasion dilatation 
of the gall bladder with dropsical 
liquid due to passive hypermia and 
condition is called dropsy of the gall 
bladder. 



GALL STONES. 203 

3. Gall Stones or Cholelithiasis, results 
from inspissation of bile or the deposit 
of various substances from the bile. 

Causes. Advanced years, female sex, 
sedentary life and high living are fact- 
ors in the etiology. Inflammations 
leading to obstruction and retardation 
of the outflow of bile and desquamation 
of epithelium with mucous forms the 
nuclei of the stone are also considered 
as causes. Bacteria also play an im- 
portant part, particularly the Typhoid 
bacillus. 

Pathologic Anatomy. The stone may 
be single or multiple. They vary in 
size from minute granules to calculi 
several cm. in diameter. If single, they 
are rounded or oval; if multiple, each 
stone is marked with facets; if formed 
in the bile dutcs they are elongated. 
The minute granules (biliary sand) are 
made up of biliary pigments in combi- 
nation with calcium salts. 

Large stones are made up of a central 
nucleus composed of epithelium or 
mucous and inspissated bile surrounded 
by a radiating and crystaline zone of 
cholesterin. This may be surrounded 
by biliary pigment. 

In some cases the stone is formed of 
biliary pigment and calcium salts. The 
stones are formed in the gall bladder or 
ducts. They may occasion no disturb- 
ance, or they may cause frequent at- 
tacks of biliary colic from their passage 
to the bowel. They may become im- 
pacted in the duct at its entrance into 
the bowel or in the mouth of the cystic 
duct. 

Various secondary changes may occur 
in the gall bladder and liver. 

4. Jaundice, or Icterus, is a discoloration 
of the skin or other parts from the 
pressure in the blood of biliary pig- 
ments. It may be divided into:— 

a, Hepatogenous (obstructive, mechan- 
ical), from catarrhal enteritis and 
colangitis. This is called catarrhal 
jaundice. It may be brought about 
by obstruction to the ducts from any 
cause. 

Congestion of the liver may lead to 
"aundice by the overfilled blood ves- 



204 PATHOLOGY. 

sels or by reabsorption of the bile, 
b. Hematogenous jaundice, once re- 
garded as due to disintegrated blood 
in general circulation, but now the 
pigment formation is recognized as 
only taking place in the liver. 
Active hemolysis is, however, an im- 
portant element and is seen in yellow 
fever, acute yellow atrophy and jaun- 
dice of the new born and various in- 
toxications. 

Some believe that the hepatic cells 
may reverse their secretion so as to 
discharge the bile into the lymphatics 
instead of the bile capillaries, but 
this is not as yet proven. 
Pathologic Anatomy. The biliary ca- * 
pillaries are distended and the he- 
patic cells are pigmented. The bile 
is absorbed by the lymphatics and 
given to the general circulation. The 
skin and external mucous membrane 
are discolored. The urine is dark 
brown or green in color. "When the 
bile fails to enter the intestine the 
stools are of a putty color. 
In the hematogenous jaundice the 
color of the stools is, to a certain 
extent, maintained. 

PANCREAS. 

1. Circulatory Disturbances. 

a. Active hyperemia occurs during di- 
gestion and acute inflammation. 

b. Passive hyperemia occurs from ob- 
struction to the portal circulation. 

c. Hemorrhage occurs as minute 
petechiae or diffuse infiltrations, 
from passive congestion or hemor- 
rhagic and infectious diseases. 
Extensive hemorrhage sometimes oc- 
curs as an idiopathic affection. 

2. Atrophy occurs from old age and 
marasmic conditions. 

3. Degenerations. 

a. Parenchymatous, from acute infec- 
tions. The organ is enlarged, soft 
and sometimes congested. 

b. Amyloid is rare. 

c. Pigmentation occurs in the atrophic 
organ of old age, hemorrhagic in- 
filtration and subsequent disorganiza- 



PANCREAS. 205 

tion of the extravasated blood. 

d. Necrosis, of small areas from hem- 
orrhage or inflammations. The whole 
organ may sometimes undergo gan- 
grenous necrosis. 

Fat necrosis is most frequently found 
in association with acute or chronic 
pancreatitis, tumors of the pancreas 
or obstruction of its ducts. It may 
occur independently. 

e. Hyaline degeneration is seen in the 
islands of Langerhans, which may 
suffer atrophy or degeneration, in- 
dependently or associated with 
chronic interstitial pancreatitis. 

4. Inflammation or Pancreatitis. 

a. Acute hemorrhagic pancreatitis oc- 
curs more frequently in young per- 
sons and is due to infection of the 
pancreas or its ducts. The pancreas 
is swollen, lobules are enlarged and 
the interlobular tissues are com- 
pressed. Hemorrhagic infiltration is 
constant, but varies in extent. 

b. Acute suppurative or necrotic pan- 
creatitis results from direct exten- 
sion of septic processes, as gastric 
or duodenal ulceration, purulent col- 
lections in peritoneum, etc., or it may 
result as an independent affection 
from the intestinal tract. 

Swelling is generally marked with 
more or less softening and some- 
times necrotic foci. Complete gan- 
grene may sometimes occur. 

c. Chronic indurative pancreatitis or 
cirrhosis may be hematogenous in 
origin, resulting from syphilis and 
alcoholism, or from prolonged irri- 
tation in consequence of entrance of 
intestinal contents or partial stenosis 
of its duct. It is analogous to 
chronic hepatitis and leads to sim- 
ilar induration or cirrhosis. 

Pathologic Physiology. There is a 
disturbance of the internal secretion 
with relation to the consumption of 
sugar. When the secretion stops or 
diminishes glycosuria or diabetes re- 
sults. 

5. Infectious Diseases. 

Syphilis, in form of diffuse induration 
or gumma ta. 



206 PATHOLOGY. 

Tuberculosis, in form of miliary tu- 
bercles in case of generalized tuber- 
culosis. 
6. Tumors. Carcinoma, sarcoma is oc- 
casionally seen and is generally sec- 
ondary. 
Cysts. 

Obstruction to the pancreatic duct from 
tumors, calculi, inflammation or con- 
tracting tissue of chronic pancreatitis 
may lead to dilatations of the duct and 
sometimes cause cystic formations. 

Pancreatic calculi are made up of a 
carbonate or phosphate of lime and are 
of irregular shape. 

PERITONEUM. 

1. Circulatory Disturbances. 

a. Hyperemia, both active and passive, 
is met with from general causes. 

b. Hemorrhage, as punctate extravas- 
ations in septic and hemorrhagic dis- 
eases and in parts of the peritoneum 
covering intense inflammatory lesions 
of adjacent parts. It may also be 
due to intense passive congestion. 
Certain intoxications, as phosphorus, 
snake venom, etc. 

Traumatism may cause large hem- 
orrhage into the peritoneal cavity. 

c. Dropsy of the peritoneum or ascites 

may occur as part of general anas- 
arca in cardiac or renal disease, or to 
obstruction of the portal circulation, 
as in cirrhosis of the liver. 

2. Inflammations of the peritoneum or 
Peritonitis. 

a. Acute Peritonitis. 

Causes. Bacteria or bacterial prod- 
ucts. Among the bacteria are the 
streptococcus pyogenes, staphylococ- 
cus pyogenes, coli communis, diplo- 
coccus pneumonia, bacillus of Fried- 
lander and the gonococcus. 
The bacteria gain entrance through 
the blood, Fallopian tubes, invasion 
through walls or perforation of the 
viscera or external walls. 
Pathologic Anatomy may be divided 
into: — 
1. Acute localized peritonitis is seen 



PERITONEUM. 207 

when bacteria escape gradually and 
in small numbers through the in- 
testine walls, or when perforation 
is secondary to the production of 
an exudate, which limits the ex- 
tent of the infection. 

It is most frequently seen in asso- 
ciation with disease of the tubes 
or uterus or in the region of the 
appendix. 

The exudate may remain fibrinous, 
but generally becomes fibrino-puru- 
lent in the later stages. In cases 
of perforative peritonitis, localized 
encapsulated abscesses are com- 
monly met with. 

The exudate may be removed by 
the pus emptying into the bowel 
or in rare cases it discharges ex- 
ternally. It may become gradually 
inspissated. The fibrinous exudate 
is frequently absorbed with remain- 
ing fibrous tissue adhesions. 

2. Acute general peritonitis results 
from the discharge of large quan- 
tities of infective matter from a 
perforation of the bowel or other 
organs, or it may be due to a 
breaking down of the fibrinous wall 
of a localized peritonitis. 

The peritoneum, particularly the 
visceral, is congested and luster- 
less, with a varying quantity of 
serous exudation. It is generally 
scanty and flakes, or thin coatings 
of fibrinous exudate appears upon 
the walls of the intestine, which are 
matted together. Later, emigration 
of leucocytes or pus cells renders 
the exudate more yellow. Adjacent 
coils of the intestine are agglu- 
tinated and pockets, containing a 
sero-purulent liquid, may be formed 
between them. 

In the most violent form of the 
local or general peritonitis the ex- 
udate assumes a putrid character 
and the deposit upon the serosa 
or the serosa may undergo necrotic 
change. 

b. Chronic peritonitis may be the ter- 
mination of a localized acute form. 
It may be due to inflammatory thick- 



208 PATHOLOGY. 

ening of the peritoneum adjacent to 
organs the seat of disease. 
If due to localized peritonitis it 
usually presents itself in the form of 
fibrous thickenings or adhesions, and 
occasionally calcareous plates are 
found in the thickened peritoneal cov- 
erings of the bowel, etc. If it is 
due to diffuse acute peritonitis the 
adhesions are widespread and the 
peritoneum is more or less diffusely 
thickened and more or less liquid ef- 
fusion may be present. In some cases 
the peritonitis arises as a chronic 
process from the beginning. The 
cause for this is obscure. Syphilis 
sometimes seems to be a factor. The 
peritoneum is uniformly thickened, 
but in some cases presents small nod- 
ular lesions, suggesting miliary tuber- 
cles. In several instances serous ef- 
fusion, have led to the diagnosis of 
tuberculous peritonitis. Microscopic 
examination shows a fibrous structure, 
and is negative to tuberculosis. 

3. Infectious Diseases. 

Tuberculosis of the peritoneum is 
usually secondary to tuberculosis of 
some abdominal viscera or of a more 
distant organ. 

It is primary in rare instances. 
Marked inflammatory changes are as- 
sociated with the specific tubercle. 
In some cases extensive adhesions are 
met with and the tubercles tend to 
agglutinate, forming considerable 

cheesy masses. 

Miliary tuberculosis without any in- 
flammatory changes may occur. 
Tuberculosis of the peritoneum may 
terminate by complete resolution, but 
the peritoneum is left somewhat thick- 
ened. 

4. Tumors. Fibromata, lipomata, sarco- 
mata, carcinoma ta (usually secondary). 

5. Parasites. Echinococcus, Filaria, Lin- 
guatula Rhinaria. Cysticercus cellu- 
losae. 



209 



DISEASES OF THE URINARY 
SYSTEM. 

KIDNEYS. 

1. Malformations. One kidney may be 
absent and in rare instances both may 
be absent. They may be congenitally 
lobulated and in some cases three kid- 
neys have been observed. The kidneys 
may be united into one horse-shoe 
shaped organ. 

They may be abnormally attached or 
may be movable or floating. 

2. Circulatory Disturbances. 

a. Anemia, as a part of general anemia 
or by pressure upon its arteries by 
growths, etc. The organ is pale and 
shows various atrophic and degen- 
erative changes. 

b. Hyperemia. 

1. Active Hyperemia is due to in- 
flammation from chemical or infec- 
tious irritation. The kidney is en- 
larged and dark red in color, with 
sometimes punctate hemorrhages. 

2. Passive Hyperemia is due to con- 
ditions impeding the circulation. 
The organ is enlarged and darkened 
in color, especially in the pyramids. 

c. Hemorrhage. Small hemorrhages 
(punctate) may occur from intense 
active or passive hyperemia, also in 
nephritis. 

Large hemorrhages are the result of 
trauma. 

d. Edema occurs from obstruction to 
the venous circulation. Congestion is 
associated. Cases of simple edema 
may result from obstruction to the 

urinary outflow. 

e. Thrombosis is rare, but embolism is 

quite common. 

3. Inflammation or Nephritis. 

Causes. Parenchyma poisons, as ar- 
senic, mercury, phosphorus, cantharidis, 
etc. Infectious diseases, as scarlet 
fever, diphtheria, cholera, septicemia, 



210 PATHOLOGY. 

etc. Chronic infections, as syphilis, tu- 
berculosis, etc., and auto-intoxications, 
as gout, etc. 
Pathologic Anatomy. 
a. Acute Parenchymatous Nephritis or 
Acute Bright's Disease. 

1. Acute Degenerative Nephritis. The 

kidney is enlarged and pale. The 
cortex is thickened and the cap- 
sule strips easily. The epithelium 
of the convoluted tubule and some- 
times the capsule of the glomeruli 
is swollen, cloudy and desquamated. 
Emigrated leucocytes and some- 
times red cells are found in the 
tubules and Malpaghian capsule. 

2. Acute Glomerulomphritis. In this 
form the glomeruli are primarily 
affected. There is a proliferation 
of the vascular endothelium within 
the tuft. Polymorphonuclear leu- 
cocytes and lymphocytes may be 
present. Hemorrhage into the cap- 
sular space and necrosis of the cells 
of the capsule and tuft may occur, 
This form occurs most commonly 
in scarlet fever. 

3. Acute Diffuse Nephritis. Ordinary 
Bright's Disease. It generally oc- 
curs as a termination to either of 
the other two forms. The kidney 
has the general characteristics of 
the other forms. The capsule strips 
easily, the organ is enlarged and 
uniformly gray or yellow in color. 
Hemorrhages may give it a dark 
red color. There is more or less 
degeneration of the epithelium of 
the convoluted tubules and Mal- 
pighian bodies. Associated with the 
epithelial changes may be evidences 
of interstitial changes, and con- 
nective tissue proliferation is also 
seen. In the cases where there is 
a hemorrhagic tendency the term 
acute hemorrhagic nephritis is often 
used. 

b. Acute Interstitial Nephritis. 

1. Non-suppurative (Acute Interstitial 
Nephritis) occurs during infectious 
diseases. The changes may be dif- 



BRIGHT'S DISEASE. 211 

fuse or in areas only. The tissues 
of the corticulo- medullary junction, 
glomerular region or those beneath 
the capsule are marked with con- 
nective tissue proliferation, leuco- 
cytes and lymphocytes. 

2. Suppurative Nephritis results from 
metastatic involvement, extension 
from pyelitis or adjacent suppura- 
tive disease. Small foci or larger 
abscesses result, which empty 
themselves into the tubules and 
pelvis and sometimes the entire or- 
gan breaks down. 

c. Chronic Parenchymatous Nephritis 

results from repeated acute attacks, 
infectious diseases, alcoholism, auto- 
intoxications, etc. The kidney is en- 
larged, capsule strips easily and the 
color is grayish or yellowish. It is 
often called large white kidney. 
The kidney may sometimes be red 
in color or areas of yellow or gray 
appearing within congested portions 
give to it the term chronic hemor- 
rhagic nephritis. 

Small cysts may form in the sub- 
stance, upon the surface by disten- 
tion of the tubules or Bowman's cap- 
sules. 

In the late stages degeneration of 
the epithelium is pronounced, the or- 
gan is light in color and interstitial 
changes render the kidney more firm 
and reduced in size. 
According to the amount of fatty 
parenchymatous change, fatty con- 
tracting kidney, or according to the 
amount of interstitial overgrowth — 
secondary interstitial nephritis, is 
often applied. 

d. Chronic Interstitial Nephritis or 
Chronic Bright's Disease, or Chronic 
Granular Kidney, results from a pri- 
mary affection, as gout, alcohol, etc., 
and as a result of arteriosclerosis. 
The arteries are sclerosed and the 
cortex of the kidney degenerates in 
patches. The kidney is hard, red, 
atrophied in areas and somewhat con- 
tracted. 

In advanced cases it is very small 



212 PATHOLOGY. 

and indurated. The surface is nodu- 
lar, capsule thick and adherent to the 
atrophied cortex. There is marked 
increase of fibrous tissue, which is 
abundant along the tubules and 
around the glomeruli, which tend to 
atrophy and may disappear. 

The epithelium of the tubules de- 
generate and disappear, to be re- 
placed by a cubical non-secreting 
form. The tubules may dilate and 
contain in many places epithelium 
undergoing fatty, granular or hyaline 
degeneration, which forms casts. 
The tubules may dilate so as to form 
cysts. 

Pathological Physiology. Gastroin- 
testinal disturbances. In the acute 
form the urine is decreased and may 
be mixed with blood. In the chronic 
form nitrogenous elimination may be 
reduced. Urea is decreased and uric 
acid is generally decreased in quan- 
tity. In all cases there is an albu- 
minuria and the presence of tube 
casts, which may be divided into: — 

Hyaline casts (clear rounded bodies), 
seen in simple congestion and in 
icterus. They are abundant in acute 
and chronic forms of nephritis. 

Cellular casts, most frequent are 
granular or hyaline casts covered with 
epithelial cells, and are seen in the 
acute parenchymatous nephritis. 
Leucocytic casts are found in puru- 
lent pyelonephritis. 

Blood casts are made up of red blood 
cells or blood pigment, and are seen 
in acute and chronic hemorrhagic 
nephritis. 

Granular casts are composed of 
broken-down epithelial cells and are 
common in chronic nephritis; may 
also occur in the acute form. 

Cylindroids are thread-like formations 
resembling casts, but have long taper- 
ing ends. They occur in irritations 
that are not sufficient to cause ne- 
phritis. They are also found in ne- 
phritis. They are also supposed to 
.. 'be produced from other parts of the 



URETERS. 213 

genito-urinary system, as from the 
glands of Cowper. 

Results of Nephritis. From the in- 
fectious or toxic cause, acute de- 
generative or inflammatory lesions of 
the heart muscle and dilatations may 
occur. Acute inflammations of the 
serous membranes. 

Subacute or chronic nephritis may 
cause hypertrophy of the heart. 
The arteries become sclerosed. 
Edema and dropsy, from disease cf 
the blood vessels. 

Uremia is the clinical manifestation, 
probably caused by the retention of 
toxic substances in the blood, which 
are ordinarily excreted with the 
urine. 

4. Atrophy may be congenital or may be 
due to old age or nephritis. 

5. Hypertrophy may take place in one 
kidney when the other is congenitally 
wanting, diseased or has been removed. 

6. Degenerations. Parenchymatous, fatty 
infiltration and degeneration, calcifica- 
tion, glycogenic infiltration, amyloid 
degeneration. 

7. Infectious Diseases. Tuberculosis and 
Syphilis. 

8. Tumors. Fibroma, lipoma, leiomyoma, 
congenital adenoma (remnant of the 
suprarenal capsule), sarcoma, adenoma 
(rare), papuliferous cystic adenoma, 
carcinoma (rare), cysts. 

9. Parasites. Bacteria occur in various 
affections. Of the animal parasites the 
echinococcus cysts, filariae, eggs of 
Fasciola hepatica, amoeba and infu- 
soria. Round worms and the oxyuris 
may migrate or enter through fistulae. 

PELVIS OF THE KIDNEY AND URE- 
TER. 

The pelvis or ureter may be absent or 
malformed. The ureter may be ob- 
structed by congenital atresia, twists 
or disease. The ureters may be dilated 
from the above causes and the secre- 
tion still going on may convert the 
kidney into somewhat of a cyst con- 
taining a clear liquid, partly urine and 



214 PATHOLOGY. 

partly transudate, to which condition 
the term hydronephrosis is given, j Cal- 
culi frequently occur in the pelvis of 
the kidney from the precipitation of 
various normal or abnormal constit- 
uents of the urine. They may vary in 
size from small particles (renal sand 
or gravel) to large stones made up of 
uric acid, oxalate of lime and some- 
times calcium carbonate and triple 
phosphates. 

Inflammation of the Pelvis, or Pyelitis, 

results from irritations of ingested 
poisons, as cantharidis, turpentine, etc., 
and more frequently from irritation of 
a calculus. The inflammation may ex- 
tend into the kidney (pyelonephritis). 
If there is complete obstruction and the 
pelvis becomes dilated and filled with 
pus the term pyonephrosis is given. 
Inflammation of the Ureter, or Ure- 
teritis, may occur under the same con- 
ditions as pyelitis. 

BLADDER. 

The bladder may be absent or divided 
by a septum; both conditions are rare. 
A common condition (exstrophy), an- 
terior wall of the abdomen over the 
bladder and the bladder is wanting and 
the ureters are exposed to view. 
Fistulous openings between the blad- 
der and adjacent cavities are often 
met with from disease or injury. Dila- 
tation may result from stenosis of its 
neck or urethra, or paralysis in conse- 
quence of disease of the spinal cord 
or nerves. Diverticulae may be ac- 
quired, which are sometimes large and 
afford concealment for calculi. 
The bladder may become hypertrophied 
from obstruction to the urinary flow. 
Rupture may take place from over- 
distention or trauma. 

1. Circulatory Disturbances. Anemia, ac- 
tive and passive hyperemia are met 
with from the usual causes, and hem- 
orrhages from severe congestion or in- 
flammation, ulceration, tumors, cal- 
culi, etc., and hemorrhagic diseases are 
also met with. 

2. Inflammation of the Bladder, or 
Cystitis, may be acute or chronic and 



BLADDER. 215 

is caused by irritants excreted with 
the urine, infections as gonorrhoea, 
etc., injury as by calculus, etc. 
It may be divided into: — 

a. Muco-purulent Cystitis. In acute 
cases the mucous membrane is swol- 
len, blood vessels are injected and 
the surface is covered with a muco- 
purulent exudate containing pus cells 
and desquamated epithelium. In 
chronic cases the submucosa is thick- 
ened and the muscularis is hyper- 
trophied and fibrous tissue bands rib 
the surface. Erosions and ulcerations 
may occur. 

b. Phlegmonous Cystitis results from 
infections or retention of the urine 
in paraplegia. Perforation of walls 
with paracystitis or phlegmonous in- 
flammation of the surrounding tissues 
may occur. 

c. Pseudo- membranous Cystitis occurs 
in severe infectious diseases and may 
present itself as typical pseudo-mem- 
branes or in combination with the 
phlegmonous. 

3. Infectious Diseases, as secondary tu- 
berculosis and in rare cases syphilitic 
ulcers are seen. 

4. Calculi are frequently found and are 
due to precipitation from the constit- 
uents of the urine as the result of 
stagnation and fermentative changes. 
They form in the pelvis of the kidney 
and gradually enlarge in the bladder. 
Foreign bodies, parasites, etc., may 
sometimes act as nuclei to the stones. 
The common varieties of stones are 
uric acid, the r phosphatic, oxalates are 
less common and cystin and xanthin 
are rare. 

5. Tumors. Fibroma, myoma, myxoma, 
adenoma, secondary carcinoma, pri- 
mary carcinoma (rare), and sarcoma is 
very rare. 

URETHRA. 

1. Inflammation of the Urethra, or 

Urethritis, may be acute or chronic. 
The acute is generally due to a specific 
micro-organism (gonococcus). It may, 
however, be non-specific from chemical 



216 PATHOLOGY. 

or mechanical irritation associated with 
infection. 

It usually affects the mucosa at or near 
the meatus and then spreads rapidly 
to the posterior parts. The mucosa Is 
congested, red, swollen, with a yellow 
or greenish purulent exudate. The 
crypts swell and are distended with a 
purulent exudate. 

Microscopically, it has the features of 
an intense purulent catarrh. 
Associated Lesions. Prostatitis, epididy- 
mitis, orchitis, purulent conjunctivitis 
when pus is brought into contact with 
the conjunctiva, gonorrheal arthritis 
and gonorrheal tenosynovitis and occa- 
sionally pericarditis, endocarditis and 
myocarditis, etc., are all caused by 
metastasis. 

Stricture in the membranous portion is 
frequent. This is a result of produc- 
tive inflammation of the mucosa and 
submucosa. 

Gleet is a slight discharge of mucous 
exudate in chronic urethritis. There is 
generally no gonococci, but occasionally 
a few may be found. The urine con- 
tains flocculent shreads (clap-threads) 
resembling cylindroids and often cov- 
ered with pus cells. 

2. Infectious Diseases. Gonorrhoeal 
urithritis. (See above and Bacterial 
Diseases). Tuberculosis. Syphilis, the 
chancre may occur, but usually under- 
goes rapid ulceration. 

3. Tumors. Small polypoid, carcinoma, 
sarcoma (rare), retention cysts. 



DISEASES OF THE DUCTLESS 
GLANDS. 

THYROID GLAND, may be congenitally 
absent in an idiot or a cretin. It may 
be undersized or of an irregular shape 
or separated into lobules. 
The gland stands in close etiological re- 
lationship to certain general conditions 
as: — 

Cretinism. The gland is congenitally 
absent, deficient, or early becomes 
functionless. It is sometimes goiter- 



THYROID GLAND. 217 

ous. The condition usually developes 
soon after birth. 

The cretin is physically and mentally 
undeveloped. The head is large, lips 
and tongue thick, subcutaneous tis- 
sue is flabby, abundant and some- 
times myxedematous. 
Myxedema. Develops in later life, 
sometimes following goiter, gumma, 
tumors, etc., of the thyroid gland. 
The eyelids, subcutaneous tissue of the 
face and neck are swollen, later in- 
volvement of the limbs and body oc- 
curs. The skin is pallid and dry, the 
hairs fall out and nervous symptoms 
are developed and the intelect dis- 
turbed. 

Graves Disease or Exophthalmic 
Goitre. The gland is enlarged; there 
is palpitation of the heart, exophthal- 
mos and muscular tremor. It is prob- 
ably due to over-production of thyroid 
secretion. Some authorities hold that 
the condition is primarily nervous. 

1. Inflammation, may be mild or severe. 
It results from trauma or infection. A 
degree of inflammation is frequently 
met with in infectious fevers as diph- 
theria, typhoid, etc. Recovery by reso- 
lution or abscess may take place which 
may rupture into the larynx or cellular 
tissue of the neck. 

2. Goiter or Struma, is the term given 
to enlargement of the thyroid gland 
resembling tumors but not classed as 
such. 

Cause. Certain localities, drinking 
water and an infectious cause have 
been considered but not demonstrated. 
Pathologic Anatomy. 

a. Parenchymatous Goitre. The glandu- 
lar tissue undergoes more or less ac- 
tive hyperplasia. The gland is gen- 
erally uniformly enlarged but may 
show lobular elevations. Cystic 
forms may occur and are designated 
as cystic goiter. Ordinarily the 
acini contain the normal amount of 
colloid material but sometimes the 
acini are greatly distended with the 
colloid material and the name colloid 
goiter is given. Connective tissue 
changes may be slight or very con 
spicuous in some cases. 
In thickening of the capsule and 



218 PATHOLOGY. 

preponderance of stroma, the term 
fibrous goitre is applied, 
b. Vascular Goitre, is applied when the 
enlargement is characterized by great 
dilatation of the blood vessels with- 
in the gland. The glandular tissue 
may not show any change or it may 
be similar to that of the parenchy- 
matous. The gland is enlarged and 
may pulsate. It is met with as an 
important pathological condition in 
many cases of Graves disease. 

3. Infectious Diseases. 

Tuberculosis, as miliary tubercles or 
caseous nodules. 
Syphilis, in form of gumma. 
Actinomycosis is rare. 

4. Tumors. Adenoma, carcinoma, sar- 
coma secondary tumors are rare. 

5. Parasites. Ecchinococcus cysts (rare). 
SUPRA RENAL GLANDS. 

1. Congenital Abnormalities. The glands 
may be congenitally absent, may be 
small or composed of separate portions 
some of which may be found within 
the capsule of the kidney, causing a 
tumor (Grawitz hypernephroma). 

2. Circulatory Disturbances. 
Hemorrhage (rare) is associated with 
hemorrhagic diseases, anemias, trau- 
matism, or obstruction to the venous 
circulation, etc. 

3. Degenerations. Pigmentation, fatty and 
amyloid degenerations. 

4. Inflammation during the course of 
infectious diseases is sometimes seen. 

5. Infectious Diseases. 

Tuberculosis, as miliary tubercules in 
the course of general tuberculosis, also 
as a fibro-caseous form in which the 
gland is enlarged, hard, nodular or 
irregular in outline. The capsule is 
thickened, the gland substance is dry, 
yellow and cheesy or puriform. This 
condition is found in the presence of, — 
.Addisons Disease, in which the skin 
of exposed parts of the body and flexor 
surfaces is characterized by a brown- 
ish pigmentation. The pigmentation is 
at first mottled then becomes uniform. 
Brownish or purplish spots are fre- 
quently seen on the mucous membranes. 
Together with this is great weakness, 



TESTICLES. 210 

stomachic disturbance and cardio- 
vascular asthenia. 
6. Tumors. Sarcoma, adenoma, carcino- 
ma, glioma and neuroma (rare), sec- 
ondary sarcoma and carcinoma. 



DISEASES OF THE REPRODUCTION 
SYSTEM. 

PENIS. 

1. Congenital Malformations. Absence is 
rare. It may be double or have , two 
canals or it may be abnormally small. 
The urethra may terminate on the un- 
der surface of the penis (hypospadias) 
or on the dorsum (epispadias). 

The prepuce may be elongated and con- 
stricted, producing phimosis. 

2. Inflammation, is due to injury or in- 
fection. 

Balanitis is term given when the glans 
is inflamed and posthitis, when the 
prepuce alone is inflamed. Conditions 
are caused by foreign substances or 
the decomposition of smegma from un- 
cleanliness. 

If the prepuce is constricted in front 
of the glans, it is called phimosis and if 
behind the glans it is called para- 
phimosis. 

3. Infectious Diseases. 

Syphilitic chancre, soft chancres or 
chancroid are frequent. 
Tuberculosis is rare. 

4. Tumors. Papilloma or condyloma acu- 
minatum occurs in association with 
gonorrhoea, syphilis, irritations, etc. 
carcinoma, sarcoma, angioma, lipoma 
and cysts. 

SCROTUM, may be imperfectly united. 
Elephantiasia is a common disease of 
the East. The scrotum may become very 
large and epithelioma is not uncom- 
mon. Dermoid cysts are sometimes 
found. ' 

TESTICLES. 

1. Congenital Abnormalities. Absence 
(anorchia) rare, small (microrchia), 
there may be one (monorchia), 
more than two (polyorchia), or they 
may be undescended (cryptorchia). 



220 PATHOLOGY. 

I 

2. Atrophy and Hypertrophy, may be 

seen from the usual causes. 

3. Degenerations, as fatty, myxomatous, 
calcification and caseation are met 
with. 

4. Circulatory Disturbances, such as ac- 
tive and passive hyperemia and em- 
bolism which may be followed by 
necrosis or gangrene has been seen. 

5. Inflammation of the testicle (orchitis), 
and the epididymis (epididymitis) are 
common. They may be acute or 
chronic and are due to injuries or in- 
fections. The infection may be due to 
extension from some adjacent part or 
to gonorrhoeal inflammation of the 
urethra. It may also be due to infec- 
tions as typhoid fever, parotitis, 
pyaemia, small pox, etc. 

The organ is swollen and hyperemic. 
A hydrocele may result from envolve- 
ment of the covering. Abscesses may 
form or the inflammation may take on 
a chronic form; the end is more or less 
complete distruction of the testicle. 
Permanent enlargment or gradual 
atrophy from chronic inflammation may 
ensue. 

6. Infectious Diseases. 

Tuberculosis of the testicle and 
epididymis is usually secondary. 
Syphilis, as circumscribed gummata. 
Lepra is met with. 

7. Tumors, Filroma, rhabdomyoma, sar- 
coma and carcinoma. The rare tumors 
are chondroma, osteoma, myxoma and 
adenoma. 

Cysts as dermoid and retention are 

met with. 
9. Parasites. Echinococcus cysts are 

rare. 
PROSTATE GLAND. 

1. Inflammation or Prostatitis, may be of 
traumatic origen but usually it is due 
to some infection as during the course 
of gonorrhoea, cystitis, proctitis, etc. 
Abscesses may result or it may be fol- 
lowed by atrophy. 

2. Atrophy, is rare before middle life but 
occurs in the aged. 

3. Hypertrophy is frequently seen in old 
age and may involve the entire gland or 
only one lobe. Enlargment may be due 



OVARIES. 221 

to a hyperplasia of the tissue or to new 

formations. Most common form is the 

hypertrophy of the glandular strutcure 

in which the epithelium and acini are 

increased. 

The fibrous tissue predominates in the 

interstitial form. 

Urination is often interfered with. 

4. Concretions, may be seen in old age, 
and vary in size from microscopic 
granules to bodies the size of millet 
seeds. 

5. Infectious Diseases. Tuberculosis in 
association with tuberculosis elsewhere. 

6. Tumors. Adenoma, sarcoma, carcin- 
oma, cysts. 

SEMINAL VESICLES. 

1. Inflammation, is usually due to some 
infection as gonorrhoea, epididymitis 
or prostatitis. A chronic inflammation 
of the vessels may result from the 
acute form and cause contraction or 
thickening of the walls. 

2. Tuberculosis, is usually secondary to 
the disease elsewhere. 

3. Tumors^ Primary carcinoma (rare), 
secondary carcinoma more common. 
Retention cysts. 

OVARIES. 

1. Congenital Abnormalities. One or 
both ovaries may be absent; they may 
be congenitally small or displaced, her- 
mia ovarii may occur or suppernumer- 
ary ovaries have been found. 

2. Circulatory Disturbances, active and 
passive hypermia and hemorrhages into 
the substance is met with. 

3. Inflammation or Oophoritis, is gener- 
ally a secondary infection and is due 
to an extension from the uterus, tubes 
or pelvic cavity or it may be carried 
by the blood. The most pathogemic 
germs are the gonococcus, streptococcus 
and the staphylococcus. The organ be- 
comes enlarged and soft. Its surface 
may be covered with serum or pus or 
abscesses may be formed within. A 
chronic form with fibrous tissue for- 
mation and subsequent contraction or 
atrophy of the organ occurs. 

Tuberculosis, may be primary but more 
commonly secondary to disease of other 
parts. 



222 PATHOLOGY. 

5. Tumors.. Carcinoma, fibroma, 
chondroma, angioma and cysts. The 
cysts may be due to non-ruptured 
Grafian follicles which go or increas- 
ing in size and contain a clear fluid 
with sometimes blood. Dilatation of the 
parovarian tubules give rise to the 
socalled Parovarian cysts. 
A c?7st of the ovary called papillomatous 
cystoma is made up of a number of 
cysts from the walls of which grow 
numerous papillae which may fill the 
cystic cavities. 

Dermoid cysts are more frequent in the 
ovary than in other parts. 

FALLOPIAN TUBES. 

1. Congenital Abnormalities. They may 
be absent, or deformed. 

2. Stenosis, may occur congenitally or 
be acquired. This may cause dilatation. 

3. Circulatory Disturbances. Active and 
passive hyperemia, and hemorrhage oc- 
curs normally during the menstrual per- 
iod and pathologically when due to in- 
fections. 

4. .Inflammation or Salpingitis, is caused 
by an infection by the gonococcus, 
streptococcus, colon bacillus and 
pneumococcus. The infection gen- 
erally extends from the uterin cavity. 
The mucous membrane is first involved 
with the formation -of an exudate of a 
mucous or purulent character depend- 
ing upon the severity. The contents 
of the tube may escape into the uterus 
or into the peritoneal cavity. The tube 
may become occluded and then dilated 
with fluids to which the terms hydro- 
salpinx, pyosalpinx, or haematosalpinx 
are given according to their nature. 
The walls may become distorted and 
thickened. They may contain small 
abscesses. 

5. Infectious Diseases, as tuberculosis 
(primary or secondary) and syphilis in 
the form of gummata or diffuse sclerosis 
may occur. 

6. Tumors. Fibroma, carcinoma, papil- 
loma, sarcoma. Cysts, as hydrosalpinx 
and small cysts of the fimbria, formed 

r in Multers ducts (hydatids of Morgagni) 

: may be seen. Tubo-ovarian cysts^are 

"formed by distention of the abo^ominal 



UTERUS. : 223 

end of the tube when the u.nbria are 
attached to the ovary. 
UTERUS. 

1. Abnormalities. Absence is rare. There 
may be congenital hypoplasia or ar- 
rested development may be due to a 
failure to increase in size at the age of 
functional activity and the name uterus 
foetalis seine infantilis is applied. In- 
complete fusion of Muller's ducts causes 
an anomaly in the uterus or vagina, 
e. g. uterus unicornus or bicornus. 
Atresia may be congenital or acquired 
by reason of ulceration or laceration. 
Malpositions as antiflection, retroflec- 
tion, antiversion, retroversion and pro- 
lapse are met with. 

2. Circulatory Disturbances. The uterus 
is physiologically hyperemic during 
menstruation and occurs pathologically 
in all forms of acute inflammation of 
the organ. 

Passive hypermia occurs from general 
venous stasis but especially from dis- 
location of the uterus which causes 
pressure upon the veins. 

3. Atrophy, occurs naturally from old age. 
It may follow frequent pregnancies and 
certain diseases and is caused by fatty 
degeneration and absorbtion of the 
muscular element. 

4. Hypertrophy, is physiologic during 
pregnancy. It may remain enlarged. It 
may occur in association with inflam- 
mation or from chronic congestion. The 
body of the uterus or the cervix may be 
enlarged independently of each other. 

5. Inflammation. 

a. Endometritis, when the mucous 
membrane is involved. It may be 
acute or chronic. The acute is 
caused by traumatism; infection by 
the gonococcus, staphylococcus, 
diphtheria bacillus, etc. It may oc- 
cur during specific fevers. 
The mucosa is swollen, congested, 
epithelium disquamating and the 
surface covered with mucopurulent 
discharge. Corpuscles exudate and 
the stroma is infiltrated with cells. 
The chronic form follows the acute 
or may be due to foreign bodies. There 
is infiltration of cells and the glands 
are enlarged. The glands may be oc- 



224 PATHOLOGY. 

eluded causing cystic degeneration. 

There is hyperplasia of connective tis- 
sue. 
b. Metritis, when the walls of the uter- 
us is involved. It is a result of an 
extension from endometritis, an in- 
fection or traumatism. 
The organ is enlarged, congested, tis- 
sue softened, blood and lymph ves- 
sels dilated, cellular infiltration. The 
walls may contain small abscesses and 
there may be thrombi in the venous 
sinuses. There is connective tis- 
sue hyperplasia. The muscular ele- 
ments may be degenerated and a 
small hard uterus results. 

6. Infectious Diseases. 

Puerperal Infections, occur during the 
puerperium and are due to the entrance 
of microorganisms, generally the 
streptococcus, but the staphylococcus, 
a bacillus resembling the coli communis, 
bacillus of tetanus and the gonococcus 

have also been found. 
Syphilis of the cervix has been seen as 
a chancre or a tertiary lesion. 

7. Tumors. Leiomyoma, lipoma, fibroma, 
sarcoma, carcinoma, papilloma, condy- 
loma, adenoma and cysts. 

VAGINA. 

1. Abnormalities, as prolapse primarily or 
in conjunction with prolapse of the 
uterus, bladder or rectum. Fistulous 
openings connecting it with adjacent 
hollow organs or malformations the re- 
sult of injury are also met with. 

2. Inflammation, Vaginitis or Colpitis re- 
sults generally from gonorrhoeal infec- 
tion but mechanical and chemical irri- 
tants may also cause it. Diphtheria, 
tuberculosis and syphilis may act as 
a cause. 

3.i Tumors. Fibroma, myofibroma, sar- 
coma, carcinoma, papilloma and cysts. 

VULVA. Injuries give rise to lacerations, 
inflammation, edema and sometimes a 
haematoma. Diphtheria, gonorrhoea, 
tuberculosis, chancres, gummata, chan- 
croids and gangrenes are met with. 
Elephantiasis, fibroma lipoma, myofib- 
roma, sarcoma, epithelioma, myxoma, 
cysts and venereal warts are the tum- 
ors usually found, -.•,.' 



MAMMARY GLAND. 82S 

MAMMARY GLAND. 

1. Congenital Abnormalities. The nipples 
may be absent or they may be multiple. 
The gland may be absent or there may 
be supernumerary glands (polymastia). 

2. Circulatory Disturbances. 

Hypermia occurs physiologically during 
the menstrual period and at beginning 
lactation, and pathologically from in- 
flammation, etc. 

Hemorrhages result from traumatism, 
sometimes it occurs from intense in- 
flammation or tumor formation. 

3. Inflammation or Mastitis. It may be 
acute (Acute Mastitis, which tends to 
suppuration) or chronic (Chronic 
Mastitis, which is a diffuse induration). 
It is generally caused by some infection 
but may be due to traumatism.. Some 
authorities claim the infection may 
reach the lacteal ducts through the 
general circulation, but the infection 
probably always enters through fissures 
about the nipple. The organisms most 
frequently found are the staphylococci 
and the streptococci. 

4. Atrophy, occurs physiologically after 
the menopause or it may be due to 
abscess or tumor formation. 

5. Hypertrophy, is sometimes seen in girls 
at puberty. All the constituents of the 
gland may be involved or dilatation of 
the lymph channels or degenerative 
changes may simulate true hypertrophy. 
Functional activity (galactorrhoea) may 
be increased. 

6. Infectious Diseases as tuberculosis and 
syphilis are met with. 

7. Tumors. Fibroma, myxoma, fibromyx- 
oma, lipoma, 

Sarcoma is frequently of the round cell 
variety and occurs as a diffuse form 
or as circumscribed nodules. It is not 
infrequently associated with fibroma 
and myxoma. 

Adenoma, may be independent or as- 
sociated with fibroma, sarcoma or 
others. Carcinoma may develop from 
the tubules or from the acini of the 
glands and is of the medullary, simple, 
scirrhous and myxomatous variety. 
Retention cysts.. are also met with. 



226 PATHOLOGY. 

DISEASES OF THE MUSCLES. 

1. Inflammation or Myositis. 

a. Acute Myositis, is divided, into — 

1. Localized Acute Myositis, is caus- 
ed by an injury or by an infection 
carried to a muscle or by extension 
of inflammation from adjacent 
parts or by obstruction to the cir- 
culation as by an embolism. 
There may be an exudation of ser- 
um into the tissue (serous myositis) 
or an extravasation of blood 
hemorrhagic myositis), or suppura- 
tion (suppurative myositis). 

There is hyperemia and swelling. 

2. Disseminated acute myositis or 
Polymysitis, is due to some in- 
fection. It has been seen in asso- 
ciation with some of the infectious 
fevers. It has probably been re- 
garded in connection with these con- 
ditions as a muscular rheumatism. 
The muscles are first hyperemic, 
followed by serous infiltration and 
leucocytic exudation. Fibers may 
undergo fatty or ganular degenera- 
tion. Coagulation necrosis and 
vacuolations may occur. 

b. Chronic Myositis, may be divided in- 
to:— 

1. Chronic Suppurative myositis, may 
result from acute suppuration and 
is often seen in association with 
tuberculosis and actinomycosis. 

2. Chronic Productive Myositis, re- 
sults from the acute type or from 
disease in the neighborhood of 
muscles or disease in the muscles 
themselves. It is characterized by 
an increase of the connective tis- 
sue. The muscle is enlarged, tender 
and firm. Degeneration of the 
muscle is in proportion to the con- 
nective tissue change. The fibers 
show cloudy swelling, hyaline 
changes or fatty degeneration, 
fragmentation or vacuolar forma- 
tion. 

3. Ossifying Myositis, is a variety of 
productive myositis in which bone 
is found in the substance of 
muscles. It occurs in muscles sub- 
jected to irritation or strain as in 



MUSCLES. 227 

the delloid muscle of soldiers and 
the adductor muscles in horsemen. 
Growths of bone may extend into 
muscles from diseased bone or 
periosteum. Nearly all the muscles 
of the body may be affected. 
The first formation is in the form 
of a small spicule which increases 
in size until the muscle may be con- 
verted into a bony mass. In some 
cases there is a connective tissue 
overproduction with less activity in 
bone formation. 
Atrophy. 

a. Neuropathetic Muscular Atrophy, 
is due to disease of the anterior horns 
of the gray matter of the cord, and, 
where this is the underlying patho- 
logic condition, the term progressive 
muscular atrophy is applied. There is 
a progressive atrophy of the muscles 
of the hands, arms, shoulders and less 
frequently the body and buttocks. 
The muscle fibers show various forms 
of degeneration. At the same time, 
reactive proliferation is seen in the 
connective tissue between the fibers. 
The muscle fibers themselves may 
proliferate extensively. 

A scondary neuropathetic muscular 
atrophy may occur in spinal diseases 
as syringomyelia, etc., and degenera- 
tions following cerebral disease which 
is similar to the primary form though 
it differs clinically. 

Injuries or disease of motor nerves 
may lead to local atrophies by sep- 
arating the muscle from the centers 
within the cord. 

b. Myopathic Muscular Atrophy, is seen 
in the young and is frequently 
heriditary. It begins in the buttocks, 
thighs or calves, sometimes in the 
shoulders. It may be divided into, — 

1. Simple atrophic form, in which the 
change is like that of the neuro- 
pathic. 

2. Pseudo hypertrophic form. The 
muscles enlarge but are soft and 
flabby. The child may look like an 
athlete but is extremly weak. There 
is considerable intermuscular pro- 
liferation of the connective tissue, 
with marked fatty infiltration. In 
some muscles, the fibers may be ac- 



228 PATHOLOGY. 

tually enlarged but it is undoubted- 
ly degenerative. 
c. Simple Muscular Atrophy, may be 
due to senility or lack of exercise. 
The muscular fibers are deminished in 
size with some connective tissue pro- 
liferation. In the senile cases, brown 
atrophy may occur. 

3. Degenerations. Parenchymatous, fatty 
degeneration and infiltration, amyloid 
(rare), calcification, coagulation necrosis 
or hyaline degeneration. 

4. Infectious Diseases. Tuberculosis (cold 
abscesses in psoas abscess) in associa- 
tion with tuberculosis of bone, lymph 
glands, etc. 

Syphilis as gummata, glanders, 
actinomycosis and anthrax. 

5. Tumors. Fibromata, myxomata, lipo- 
mata, osteomata, chondroma and sec- 
ondary carcinoma. 

6. Parasites. Trichinosis, cysticercus in- 
vasion and hydatid disease. 

DISEASES OF THE BONES. 

1. Rickets or Rachitis, is a constitution- 
al condition attended with overproduc- 
tion of the cellular elements of the 
bones and lack of their normal calcifi- 
cation. 

Causes, are obscure, though it is gen- 
erally conceded that there is some in- 
herited tendency with a lack of proper 
nourishment and unhygienic conditions. 
The disease generally begins during the 
first j'ear of life and continues through 
the second and third years. 
Pathologic Anatomy. The production of 
cellular elements of bone is increased, 
especially at the epiphyses. The bones 
are enlarged and tender at the ends. 
There is also a deficiency in the for- 
mation of bone. The bones of the 
skull and long bones are soft and easily 
bent and deformed. The fontanelles 

'remain open a long time. Osteophytes 
may form and the skull bones remain 
soft (craniotabes). The anterior ends 
of ribs are enlarged and form a row of 
nodes (rickety rosary). The chest is 

. often pigeon breasted. 

I When the calcification commences it 



BONES. 229 

is greater than normal and the bones 
are thus too hard, deformed and en- 
larged in places. The vertebrae and 
pelvic bones are markedly deformed. 
2. Inflammations. 

a. Periostitis, is an inflammation of the 
periosteum. 

Causes. Traumatism, by giving di- 
rect entrance to infections or by 
lowering the resistance of an area 
with subsequent infection. 
Hematogenous infection without local 
injury is often seen. 
Infective periostitis may result from 
extension of inflammation in the 
neighborhood of bones or from 
osteomyelitis. More or less periostitis 
occurs in all forms of bone diseases. 

Pathologic Anatomy. 

1. Simple Periostitis. The periosteum 
is swollen, red, and may be in- 
filtrated with blood. There is round 
cell infiltration and proliferation of 
the periosteal tissue. If the process 
is extensive andl long continued, 
fibroid thickening is observed. 

2. Purulent Periostitis, may be cir- 
cumscribed or diffuse and is due to 
some pyogenic organism acting 
through the blood. The condition 
extends rapidly, involves the bone 
and usually the medulla. Soon after 
the beginning of the inflammation, 
the periosteum is destroyed and 
more or less of the bone may ne- 
crose. The periosteum throws out 
new bone which may form a sheath 
around the necrosed portion. 

3. Ossifying Periostitis or Chronic 
Periostitis. Occurs in association 
with chronic osteitis. It is met 
with principally in syphilis. There 
is a proliferation of the osteogenetic 
layer of the perosteum, then partial 
ossification and complete bone for- 
mation with firm attachment to the 
bone. Bony excrescences, exostoses 
or osteophytes are formed. 

In some cases of pulmonary tuber- 
culosis, there is a toxin in the blood 
that gives rise to a periostitis in 
the extremities to which the term 
hypertrophic osteo-arthropathy is 
^ sometimes given. 



230 PATHOLOGY. 

b. Osteitis. (inflammation of the 
bones), is frequently caused by in- 
juries, periostitis, or other inflamma- 
tory diseases. It is also caused by 
febril diseases and occurs in rheu- 
matism, syphilis and tuberculosis. 
Acute infective inflammation is also 
met with. The blood to part is in- 
creased. The vessels of the bone, 
periosteum and medulla enlarge. The 
Haversian canals become vascular and 
capillary loops are formed. Spaces 
are formed in the bone by the soft- 
ening and absorbtion of its sub- 
stance. Contained within the spaces 
is granuation tissue and large multi- 
nuclear cells which assist in the ab- 
sorbtion of the bone and convert it 
into a cancellous condition. During 
this time at the medulla and the 
periosteum, new bone is being formed 
in which are numerous osteoblasts en- 
gaged in the bone formation. If the 
inflammation is limited in extent and 
duration, the new bone may be ab- 
sorbed. If the inflammation is pro- 
longed, the new bone becomes or- 
ganized and is denser than normal 
(osteosclerosis or condensing osteitis). 
If the process is acute, an abscess 
may be formed and if very acute the 
circulation of the periosteum and 
Haversian canals are obstructed by 
the exudates and oedema results 
which ends in necrosis. 
A disease which is a form of osteoscl- 
erosis causes irregular thickening 
and enlargment of the bones of the 
head and face is designated as 
leontiasis ossium. 

Osteitis Deformans. Cause obscure. 
Some trophic disturbance plays a part. 
It is a condition which affects the 
skull, vertebrae and certain long 
bones, causing enlargment and elas- 
ticity on account of which there is 
great deformity. The compact bone 
is absorbed with confluence of the 
Haversian canals and formation un- 
* calcified osseous tissue. The medul- 
lary canal is filled with vascular con- 
nective tissue and pus cells. Giant- 
cell sarcoma may occupy the medulla. 
Osteomy litis. In the acute form of a 
single type as fractures and amputa- 
tions, there may be enough bone to 
close the medullary canal and adja- 



BONES. 231 

cent bone undergo rapid suppuration 
and necrosis. 

The chronic form leads to bone thick- 
ening along the medullary canal and 
to its narrowing which may go on to 
occlusion. In some cases there is 
chronic suppuration and necrosis. 

3. Atrophy, may result from disease as a 
paralyzed extremity or from a bone not 
in use by reason of deformity or in- 
jury; severe cachexia or long confine- 
ment to bed, chronic disease of joints. 
Disturbance of trophic nerves and cer- 
tain nervous conditions as cretinism and 
insanity have been met with as a cause. 
There seems to be an idiopathic form 
which brings on a condition of bone 
fragility (fragilitas ossium or osteop- 
sathyrosis) from the increase of its 
narrow spaces and general porosity. 

4. Hypertrophy. A local hypertrophy may 
be caused from muscular development 
and exercise or strain on the bone. 
Giantism. Certain bones or the bones 
of the entire skeleton may be involved. 
The bones are enlarged, thick and ir- 
regular. The condition usually begins 
about puberty. 

Acromegaly, is allied to giantism but 
the bones of forearms, hands, legs, feet, 
upper and lower jaws and the nose are 
marked in their enlargment. The 
etiology is obscure through enlarg- 
ment of the pituitary body, also the 
persistence of the thymus gland has 
been considered as factors but this is 
still unsettled. 

5. Degenerative Conditions. 

a. Necrosis, is due to periostitis, 
osteitis and osteomyelitis, which leads 
to an interruption of the blood sup- 
ply to the bone. Embolic obstruc- 
tion of the blood vessels may also 
cause it. The more acute and intense 
the inflammatory process the more 
likely is the necrosis. 
The surface, cancellous portion or the 
entire thickness of the bone may be 
involved. The line of demarkation of 
the living bone with that of the dead 
bone is softened and rarified, and 
granulation tissue is formed. These 
processes go on until the dead por- 
tion (sequestrum) is loosened. The 
periosteum is forming new bone which 



232 PATHOLOGY. 

may encase the sequestrum and pre- 
vent its escape, unless this is 
brought about through openings or 
cloacae that exist in the new bony 
case. A peculiar form of necrosis is 
produced by phosphorus fumes and 
affects the maxillary bone. 
Syphilis and tuberculosis may also 
produce necrosis. 
b. Osteomalacia, is a disease of adult 
life and is most frequently seen in 
females, particularly in the puerperal 
woman. The real causes are not 
known. The bone salts are absorbed, 
the medullary and Haversian canals 
are enlarged, the bone trabecullae dis- 
appear and the corticular layer be- 
comes thin. 

The long bones contain red narrow 
and fractures readily. In the later 
stages the bone becomes soft and 
bends quite easily. Deformities may 
become great. During the late stage 
there is only a jelly-like substance 
within the periosteum. It proves fatal 
in about two years. 

5. Infectious Diseases. 

a. Tuberculosis, is more frequent in the 
young and may be acute or chronic. 
The tubercles are found in the 
periosteum, the bone or the medulla. 
The cancellous tissue is particularly 
liable. The areas are gray in color, 
surrounded with congested and swol- 
len tissue. Caseation of area takes 
place. Bone trabecular are broken 
down. Giant cells are found in the 
tubercles, osteoclasts appear on the 
bone lamella and granulation tissue 
is formed. 

By extension new foci are formed. 
The diseased bone may separate 
through caseation and caries is the 
usual course. The inflammatory pro- 
cess may produce an abscess which 
sometimes invades the soft parts as a 
cold abscess (psoas abscess). The 
tubercular bone abscess has generally 
a pyogenic membrane and the con- 
tents of the abscess may be cheesy 
matter or pus. Tuberculosis of the 
bones has a tendency to invade the 
. joints. 

b. Syphilis. The periosteum is fre- 
: . quently involved. There is thicken- 



JOINTS. 233 

ing, with an infiltration of cellular 
matter which may undergo gummy 
or mucoid degeneration and super- 
ficial necrosis. 

Syphilis of the bone attacks the can- 
cellous tissue mainly. The gumma- 
tous material extends into the Haver- 
sian canals, erode the bony, lamellae 
and enlarge the canals, thus giving 
to the bone a worm eaten appear- 
ance. The bone is thickened near the 
gummatous formation, becomes 

sclerosed and necrosed with forma- 
tion of sequestra. The gumma may 
form in the medullary canal or ends 
of bones and invade the joints. 
In congenital syphilis, there is char- 
acteristic alterations at the junction 
of the epiphyses with the diaphyses of 
the long bones. The epiphyses may 
be completely seperated from the 
shaft. Nodes are often formed 
around the anterior fontanells and 
the nasal bones are often diseased as 
in the tertiary form. 
6. Tumors. Exostoses, fibroma, lipoma, 
myxoma, angioma, chondroma, osteo- 
ma, sarcoma, carcinoma (usually sec- 
ondary), and cysts, in connection 
with tumors and hydatids occasionally. 



DISEASES OF THE JOINTS. 

1. Inflammation. 

a. Acute Arthritis, is due to trauma; 
disease in vicinity or hematogenous 
which may occur in the course of 
infectious diseases as scarlet fever, 
small pox, pyemia, etc. Acute 
articular rheumatism may also be 
added to this group. 
It may be of a dry or fibrinous, a 
serous and a seropurulent nature. 
The synovial membrane is congested, 
the cartilages and ligaments are also 
more or less involved. The term 
synovitis implies synovial involve- 
ment and panarthritis is a general 
involvement. Fibrin is deposited on 
the surface in the dry form. In the 
serous form, the exudation is purely 
serous while in the real seropurulent, 
form, empyema of the point results. 
Resolution takes place in mild cases. 



234 PATHOLOGY. 

In the severe cases, the articulating 
cartilages may ulcerate or necrosis 
may result, leading to ostitis or 
osteomylitis. Disorganization of 

joints may take place. 

b. Chronic Arthritis may be due to 
the acute. It also '^occurs in the 
course of gout and certain nervous 
diseases. It may be divided into, — 

1. Chronic Serous Arthritis, or 
Hydrops articulorum. The synovial 
membrane is thickened and more 
or less injected (synovitis pannosa). 
The joint is filled with thin syn- 
ovia. 

2. Chronic puruient arthritis is due 
to infection, and is the outcome 
of an acute sero-purulent or puru- 
lent arthritis. It terminates in ex- 
tensive disorganization of the 
joint. A fibrous ankylosis is the 
favorable outcome. 

Arthritis deformans or rheumatoid 
arthritis, is generally seen in those 
past middle age. The cartilages 
are softened, ulcerated or eroded 
and have an irregular rough sur- 
face. Hyperplasia of cartilage cells 
takes place with subsequent degen- 
eration and absorption. The car- 
tilage is reduced and the ends of 
the bones are bare. The synovial 
membrane and ligaments thicken, 
the articulating surface is absorbed 
and proliferated in the form of ex- 
ostoses and osteophytes, and the 
joint is deformed and thickened. 
Subluxations are common and an- 
kylosis may follow. 
It is seen in the metacarpophalan- 
geal joints of hands and feet. 
Other joints may be involved. 

c. Chronic dry arthritis, with ulcera- 
tion or senile arthritis, is similar to 
the rheumatoid arthritis, but more 
slow. It is common in the hip joint. 
There is gradual absorption of the 
cartilages and exposed surfaces of 
the bone, with subsequent sclerosis 
and hyperplasia of the surrounding 
bone. 

d. Neuropathic arthritis resembles the 
other forms, but is very slow. It is 
seen in the course of spinal diseases 
such as locomotor ataxia and sy- 



BRAIN. 235 

ringomyelia. It is painless and sug- 
gests a degeneration or trophic dis- 
order. 

3. Gouty Arthritis. There is a deposit of 
crystals of the urate of sodium and 
calcium in the cartilage cells and inter- 
cellular substance of the articulations. 
The deposit may also take place in the 
connective tissue of the joints in more 
severe cases. The deposit gives rise 
to the attacks (gouty paroxysm) 'which 
is marked by inflammatory processes 
in the joint. The synovial membrane 
is hyperemic, with serous effusion and 
sometimes inflammatory manifesta- 
tions. The cartilages may become 
eroded and suppuration may take place. 
The metatarso-phalangeal joint of the 
great toe is particularly liable to be 
involved. 

4. Infectious Diseases. 

Tuberculosis, when primary, begins in 
the synovial membrane. It may be 
secondary to tuberculosis of bone when 
any part of the joint is first involved. 
The former is usually the case in chil- 
dren and the latter in adults. 
Syphilis may occur in the hereditary 
form. In later life gummata may in- 
vade the joint. 

5. Tumors. Sarcoma, exostosis, hydatids 
(rare). 

TENDON SHEATHS AND BURSAE. 

Tenosynovitis and Bursitis is like the 
inflammation of joints. 
House- maid's knee is a chronic bursitis 
with dropsical effusion, due to chronic 
irritation, and is analogous to hydrops 
articulorum. 

Ganglion is a condition of the tendon- 
sheaths which presents itself as a 
rounded cystic nodule on the back of 
hands and wrist. It is due to a local- 
ized dropsical condition of the tendon 
sheath. 

DISEASES OF THE BRAIN AND ITS 
MEMBRANES. 

BRAIN. 

1. Circulatory Disturbances. 

a. Anemia. Acute anemia results from 
severe hemorrhage or hyperemia in 



236 PATHOLOGY. 

other parts of the body. It is sup- 
posed to exist in fainting, during 
hysterical crises and in sleep. 
Chronic anemia occurs in severe 
cachexias and sometimes in atheroma 
of the cerebral arteries. 
Local anemia may result from throm- 
bosis and embolism. 

b. Hyperemia is associated with in- 
flammatory or toxic conditions. 

1. Active hyperemia may be divided 
into, — 

Local active hyperemia, usually as- 
sociated with meningitis, and may 
be limited to the superficial part 
of the cortex. It may also occur 
after thrombosis. 

General active hyperemia is sup- 
posed to be associated with un- 
usual activity of the mind. 
In acute infections, such as typhoid 
fever, excessive irritation of the 
cerebral substance may occur, 
which gives rise to symptoms some- 
what like those of meningitis. It 
is termed meningismus and is due 
to hyperemia. 

2. Passive hyperemia is associated 
with valvular heart disease or 
chronic lung disease, or may be 
caused by tumors pressing upon the 
jugular vein, or intracranial condi- 
tions, as brain tumors, etc. "Where 
passive hyperemia exists there is 
nearly always edema of the brain. 
Apoplexia serosa is a local edema 
of the brain found near the areas 
of softening. 

c. Apoplexy may be divided into three 
varieties. In all varieties there is a 
thickened intima and muscular coat, 
causing obliteration of the vessels or 
an atheromatous condition, with the 
formation of thrombi on the rough- 
ened surface, or give rise to aneu- 
rysmal dilatation of the vessel. Por- 
tions of brain with occluded or rup- 
tured vessel and formation of clot 
gives rise to well-marked focal symp- 
toms. 

Apoplexy is due to, — 
1. Hemorrhage (cerebral hemorrhage) 
may be divided into, — 



BRAIN. 237 

Punctate hemorrhage, due to al- 
teration in walls of blood vessels 
or of the degree of blood pressure, 
causing extravasation of blood into 
surrounding tissues. The principal 
causes are hyperemia and disease 
of the vessel walls. 
Massive hemorrhage occurs usually 
from the branches of the middle 
cerebral artery, which are the fre- 
quent seats of miliary aneurysms. 
The blood collects in the form of 
an irregular dark mass. The size 
of the clot varies with its location 
and the amount of extravasated 
blood. The time of the absorption 
of the clot varies according to its 
size. It begins to lose its color in 
two or three weeks, and in about 
twelve weeks it is reduced to a 
yellowish mass. The damaged brain 
tissue undergoes fatty degenera- 
tion. 
2. Thrombosis and Embolism. 

Thrombosis probably occurs most 
frequently in the basilar artery, 
while embolism occurs in the ar- 
tery of the Sylvian fissure. That 
portion of the brain deprived of its 
blood supply undergoes fatty de- 
generation. The area becomes yel- 
lowish and is known as yellow 
softening. The embolism may be- 
come infected, as in ulcerative en- 
docarditis and pyemia, so that in 
addition to the pathological changes 
already present inflammatory proc- 
esses are set up. 
2. Inflammation. 

a. Encephalitis is an acute inflamma- 
tion, which is probably of an infec- 
tious origin. It occurs during the 
course of scarlet fever, measles, 
pneumonia, influenza, etc. It may be 
limited to large or small areas, and 
many foci of inflammation may be 
present. In the affected parts the 
neurones are found to be degen- 
erated. In the course of time the 
tissue becomes sclerosed, and if a 
system of neurons are destroyed 
symptoms, as imbecility, paralysis of 
muscles, defect in speech, etc., en- 
sues. If only a few neurons are de- 
stroyed partial recovery may take 
place by the absorption of the small 



38 PATHOLOGY. 

clots and infiltrations. The gHa and 
connective elements are increased 
and sclerosed patches follow the at- 
tempts at repair. Adhesions between 
the meninges and cortex may be 
formed. 

Cerebral abscess may be caused by 
an injury with or without a fracture. 
An abscess may form several weeks 
after an injury. Otitis media of the 
chronic form is the usual cause of 
abscess. An abscess may also result 
by metastasis from some other part 
of the body. 

Single abscesses are generally of slow 
growth, large in size, with a thick 
capsule. Small abscesses are usually 
numerous and are of metastatic form. 
An abscess may be latent for years, 
is never absorbed and ruptures into 
the ventricle or on the surface of the 
brain, which is frequently followed 
by meningitis and thrombosis of the 
sinuses. i 

The micro-organisms found in the 
pus are the streptococci, staphylo- 
cocci and pneumococci. Occasionally 
the bacillus pyocyaneus and the tu- 
berculosis. 
b. Meningoencephalitis, or General Pro- 
gressive Paralysis, is more common in 
men than in women. Syphilis seems 
to play an important part in its eti- 
ology. In addition excesses in alcohol 
and sexual indulgence is also consid- 
ered as a cause. 

The meninges are hyperemic and 
many capillaries are occluded. The 
vessels cell elements are overpro- 
duced. Vessels dilate and fibrous tis- 
sue are formed around them. There 
is a degeneration of the neurones and 
the nucleated cells of the neuroglia 
are increased. 

The cortical cells and their dendrites 
undergo fatty degeneration. 
The changes in the neuroglia, cere- 
bral cells and the vessels cause a gen- 
eral atrophy of the brain. The en- 
tire brain may lose one-fourth its 
weight. The meninges become thick- 
ened and the cerebral fluid is in- 
creased in quantity. There may also 
be sclerosis of the posterior columns 
of the cord. 



BRAIN. 239 

The disease is not directly due to 
syphilis, but an attack of syphilis 
generally precedes it. Some cases 
fail to give any syphilitic history. 
c. Chronic encephalitis is a variety of 
sclerosis, but may take on a scar 
formation. 
It may be divided into, — 

1. Lobar sclerosis is usually an ex- 
tensive but circumscribed process 
affecting the whole or part of one 
or more lobes of the brain. The 
affected area is usually diminished 
in size. The consistency is greatly 
increased, the tissue is almost like 
cartilage. 

Microscopically, there are some 
changes found in other forms of 
sclerosis. The cause seems to be 
due to some fetal vascular disturb- 
ance. 

2. Multiple, Insular or Disseminated 
Sclerosis. Cause is obscure. The 
greater number of authorities be- 
lieve it to be of vascular origin, 
i. e., the patches are due to some 
toxic agent, while some think it due 
to an overgrowth of neuroglia and 
that myelin fibers suffer from pres- 
sure; others think it is a defect 
in the development of the nerve 
fiber, with the medullary sheath 
imperfect or wanting. 

There are many small patches of 
sclerosis scattered through the cen- 
tral nervous system. The patches 
vary insize and are irregular in 
shape. They occur in the cortex, 
but most frequently in the central 
white matter of the brain. The 
basal ganglia are common seats. In 
the cord the patches involve several 
tracts. There is no secondary de- 
generations in the affected tracts, 
as the process does not affect the 
axones. The neurone sheath and 
the adventitious tissue of the brain 
and cord are not sclerosed unless 
the gray matter is involved. The 
patches are more vascular than the 
normal tissue and are of pink color; 
in the later stages they become 
nearly white. The blood vessels are 
thickened. 
If a patch extends to the gray mat- 



240 PATHOLOGY. 

ter there is fatty degeneration of 
the cell elements. The nerve fibers 
as they pass through the patches 
are compressed and reduced in size. 
The medullary sheath is interrupted 
and undergoes fatty degeneration 
and an occasional axon is de- 
stroyed. 

3. Infectious Diseases. 

Tuberculosis occurs in the form of mili- 
ary tubercles, or the so-called solitary 
tubercle, or tyroma, which is made up 
of a rounded mass of grayish or yellow 
color, showing fresh gray tubercles at 
the periphery. Early caseation is usual. 
Syphilis, as gummata or as a diffuse 
vascular disease, with secondary de- 
generation and softening or sclerosis of 
a diffuse or focal character. 
Actinomycosis is secondary and may 
take the form of a chronic abscess or 
may be tumor like. 

4. Tumor. Glioma, sarcoma, fibroma 
lymphangioma, osteoma, p'sammoma, 
carcinoma. Cysts in connection with 
other cysts or may sometimes be para- 
sitic in origin. 

VENTRICLES. 

Hydrocephalus is an excess in quan- 
tity of the cerebro-spinal fluid in the 
ventricles. It may be either external 
or internal. The external is caused by 
exudation of serum from the meninges 
and the internal is caused by the ac- 
cumulation of fluid in the ventricles. 
Hydrocephalus may be divided into, — 

a. Acute, which is caused by a menin- 
gitis. 

b. Chronic, which is usually caused by 
a mild meningitis and the obstruction 
of the outlets to the ventricles at the 
aqueduct of Sylvius and the foramen 
of Munroe. 

THE MEMBRANES OF THE BRAIN. 

Dura Mater. 

1. Circulatory Disturbances. Active and 
passive hyperemia occur in association 
with gumma, tumors and other focal 
diseases; while hemorrhages are usually 
due to trauma and are extra or intra- 
dural. A collection of . blood between 
the skull and the dura is sometimes 
- called internal cephalhematoma. 



MENINGES. 241 

2. Inflammation or Pachymeningitis may 

be acute or chronic and is divided 
into, — 

a. Hemorrhagic Pachymeningitis is 

found more often in the aged than 
in the young. Alcoholism and trauma 
are etiological factors. 
A grayish membrane, with brown 
spots composed of hematoidin, ap- 
pears on the inner surface of the 
dura. Later there is diapedesis of 
blood corpuscles or actual hemor- 
rhage may occur. 

b. Suppurative Pachymeningitis occurs 
in consequence of trauma, caries or 
other disease of the skull. Sometimes 
it may be due to internal or middle 
ear disease. 

c. Productive Pachymeningitis is of a 
fibrous or ossifying character. It may 
follow the two other forms. 

3. Infectious Diseases. 

Tuberculosis is in form of miliary tu- 
bercles, in association with disease else- 
where. It may be primary in some 
cases. 

Syphilis, as a diffuse productive pachy- 
meningitis or gumma. 

4. Tumors. Alveolar sarcoma, angiosar- 
coma, fibroma, small round cell sar- 
coma, gliosarcoma and carcinoma. 
Cysts, as meningocele. 

The Pia and Arachnoid. 

1. Circulatory Disturbances. 

Anemia, active and passive hyperemia 
from the usual causes. Hemorrhages, 
as small punctate in meningitis, 
scurvy, purpura, etc.; large are found 
between the pia and arachnoid from 
trauma and rupture of aneurysms. 
The blood may become inspissated, or 
it may be encapsulated with absorp- 
tion of pigment, causing a cyst (hy- 
groma). Edema of the membranes 
or collections of liquid in the sub- 
arachnoid space may be due to pas- 
sive congestion. 

2. Inflammation, or Leptomeningitis, is 
always infectious and may be acute or 
chronic. 

a. Septic meningitis occurs during the 
course, of septic disease or wounds. 
It may appear during pneumonia, ty- 



242 PATHOLOGY. 

phoid fever, eruptive fevers, emv 
pyema, erysipelas and ulcerative en- 
docarditis. The germs usually found 
are the streptococcus, staphylococcus 
and the pneumococcus. 
A part or the entire membrane may 
be affected. The convexity of the 
brain is more likely to suffer. 
There is hyperemia at first, then an 
exudation of serum, which may cause 
oedema of the cortex and separation 
of the layers of the meninges. 
Fibrin is also deposited as flakes on 
the pia, and pus collects in the 
meshes and on the surface of the 
membrane. 

Abscesses of the cortex may form and 
the inflammation may extend into the 
ventricles. 

Tuberculosis and syphilis also cause 
a meningitis. (See Infectious Dis- 
eases below). 
b. Epidemic Cerebro-Spinal Meningitis, 
or Spotted Fever, results from an in- 
fection by the diplococcus intra- 
cellularis • meningitidis of Weichsel- 
baum, and in this is its only differ- 
ence from the septic form. The In- 
flammatory process generally begins 
on the frontal lobes and extends back- 
ward and downward, the basal menin- 
ges being involved late in the course 
of the disease. 

3. Infectious Diseases. 

Tuberculous Meningitis is usually a 
secondary infection. The base of the 
brain is more likely to suffer, the spaces 
become filled with tubercles and inflam- 
matory products. Rarely there is pus; 
but the pia is studded with tubercles, 
and there is exudation of fibrin, lymph 
and serum. The closure of the fissure 
of Sylvius will cause the ventricles to 
become greatly distended. 
Syphilitic Meningitis. The meninges 
near the crura is the favorite location. 
It occurs in the form of gummatous 
infiltrations. 

Flattened nodular thickening of gray or 
pinkish color, with a tendency to ne- 
crotic change, appear in the arachnoid 
and pia. 

4. Tumors. Pacchionian bodies, endothe- 
lioma, cholesteatomata, lipoma and 
teratomata. 



243 



DISEASES OF THE SPINAL CORD 
AND MEMBRANES. 

THE SPINAL CORD. 

1. Congenital Abnormalities. Absence 
(amyelia) exists only with anen 
cephalus. The cord may be abnormally 
small (micromyelia) ; it may be double 
(diastematomyelia); it may be of un- 
usual length; it may be heterotopic, 
i. e., a doubling of one of the horns, or 
disorganization of one or both horns, 
or of fissures extending into its sub- 
stance; the central canal of cord may be 
dilated; the imperfect closure of the 
posterior processes of the vertebrae 
may give rise to clefts, which are known 
as rachischisis, and if the membranes 
of the cord protrude to form a sac or 
hernia it is called spina bifida. 

2. Circulatory Disturbances. 

a. Hyperemia may be present. It may 
result from long decubitus and in 
early stages of inflammations of the 
cord and meninges. Excessive venery 
may also cause it. 

b. Anemia arises from narrowing of the 
vessels in meningitis or occlusion of 
the vessels by embolism, also by rea- 
son of a general anemia. 

c. Varicose Veins are sometimes found 
as a sort of plexiform angioma. This 
has been seen sometimes after birth 
and is frequently seen in myelitis and 
sclerosis. 

d. Hemorrhages are rare. They occur 
from injury and in connection with 
myelitis or in death by drowning or 
strangulation. Minute extravasations 
are found in the white and gray mat- 
ter from asphyxial states. Large 
hemorrhages, not due to injury, be- 
gin in the gray substance. The blood 
clot may lacerate the tissues. 

The irritation caused by hemorrhages 
is followed by inflammatory reaction. 
A condition in which the central canal 
is dilated and contains blood is called 
hematomyelia. It results from trau- 
matism or some vascular degenera- 
tion 



244 PATHOLOGY. 

3. Inflammation. 

a. Myelitis may be divided into, — 

1. Acute Myelitis is due to pressure 
on the cord by tumors or from a 
curvature of the spine, or injuries, 
violent muscular action, exposure to 
cold, toxic blood conditions or ex- 
cessive functional activity. 

At first the vessels are dilated and 
gives the part a red color (red soft- 
ening). The coloring matter of 
the blood extravasations undergo 
changes and yellow softening ap- 
pears. Later the cord becomes 
grayish from absorption of products 
of fatty degeneration. 
The nerve fibers are degenerated 
early into masses of myelin and 
granular matter, which contains red 
and white cells and fragments of 
axis cylinders. 

The gray matter contains round 
cells, nuclei of other cells, and the 
tissue is very granular. The nerve 
cells are swollen and contain fatty 
matter, while their processes are 
small or have disappeared. The in- 
terstitial tissue takes on a fibrous 
appearance, with the nerve pro- 
cesses of Deiter's cells extending 
between the nerve elements. The 
myelin sheaths are degenerated to 
a varying degree, and the axis cyl- 
inders are granular and swollen. 
As the disease progresses the gray 
matter disappears and the perivas- 
cular exudate shows fatty degenera- 
tion. 

In the gray degeneration vacuoles 
are found in the neuroglia. 

2. Chronic Myelitis develops slowly 
and ma- be due to the acute form, 
repeatea exposures to cold, various 
injuries, a hereditary tendency, 
continued over-exertion, tumors, 
chronic disease of bones, meningitis, 
alcoholism, gout and syphilis may 
all act as etiological factors. The 
cord is wasted. The white matter 
seems grayish and the gray matter 
dark. It may be transverse or dis- 
seminated. There may be several 
isolated foci of disease, or there 
may be a sclerosed ring around the 
cord. The disease is interstitial, the 



SPINAL CORD. 245 

connective tissue is increased, with 
but few nerve elements present. 
In some part of white matter the 
interstitial tissue is increased and 
contain nuclei and various shaped 
cells. Deiter's cells are often pres- 
ent. As the condition progresses 
the nerve fibers and cells gradually 
disappear, and the axis cylinders 
are of irregular shape and break 
up in portions. 

The blood vessel walls are thick- 
ened and ganglion cells swell, then 
shrink, become irregular, lose their 
projections and disappear. 

b. Polyiomyelitis, or Atrophic Spinal 
Paralysis, may be divided into, — 

1. Acute Anterior Polyiomyelitis, In- 
fantile Paralysis, or Acute Atrophic 
Spinal Paralysis, occurs almost ex- 
clusively in young children. It is 
undoubtedly due to some blood 
state. It appears after some ex- 
posure to cold subsequent to some 
other infectious disease and has ap- 
peared as an epidemic. The nature 
of the poison is unknown. There is 
an acute inflammation of the an- 
terior cornua of the cord. The ves- 
sels are distended and minute ex- 
travasations into the substance may 
be seen. 

The neuroglia is swollen, ganglion 
cells are granular and the processes 
indistinct. Granular corpuscles. 
If the cervical and lumbar enlarge- 
ments are involved there is soften- 
ing. 

If the process is slight there may 
not be much destruction of 
nerve elements. The inflammatory 
changes extend into other portions 
of the cord and cause degeneration 
of other tracts, especially the lat- 
eral. In severe cases the motor 
nerve cells almost entirely disap- 
pear, with later distinct degenera- 
tion of their nerve fibers. 
The cord at the diseased level is 
reduced in size. The muscles sup- 
plied by the diseased nerves are 
paralyzed and undergo atrophy. The 
muscles may contract and give rise 
to various deformities in the limbs. 

2. Chronic Poliomyelitis, Chronic 



246 PATHOLOGY. 

Spinal Muscular Atrophy, Progres- 
sive Muscular Atrophy, Wasting 
Palsy, is most frequent between the 
ages of 25 and 45 years. It results 
from a slow degeneration of the 
motor cells in the anterior cornua 
of the cord. There seems to be a 
hereditary tendency in its etiology, 
but prolonged emotional excitement, 
and syphilis seems to bear some 
connection to it. 

The motor cornual cells are atro- 
phied, the nerve fibers are degen- 
erated and the muscles supplied by 
these nerves undergo wasting. The 
disease is probably a degeneration. 
The muscles are reduced in size 
and are pale. The muscle fibers 
may be narrowed or they may un- 
dergo fatty degeneration and have 
disappeared in some instances. 
In many of the nerve fibers the 
myelin undergoes fatty change and 
the axis cylinder disappears, noth- 
ing but connective tissue threads 
remain. 

The affected portions of cornua are 
wasted and softened. 
The ganglion motor cells are 
changed in outline with loss of their 
processes or the cells have disap- 
peared. 
Posterior Sclerosis, Locomotor Ataxia, 
Tabes Dorsal is, occurs generally be- 
tween the ages of 20 and 50 years. It 
is more frequent in the male than the 
female. Syphilis can be traced as a 
cause in from 70 to 90 per cent, of 
the cases. Exposure to wet and cold 
and excessive fatigue have been ad- 
vanced as a possible cause. There is 
a degeneration of the central and peri- 
pheral sensory nerve elements. The 
posterior columns of the cord are of 
a graj r ish color, due to an over-pro- 
duction of connective tissue. The 
columns are reduced in size. The de- 
generation of the nerve elements and 
the increase of connective tissue are 
confined mainly to the posteromedian 
columns, but other columns, espe- 
cially those of the lumbar region, may 
be involved to some extent. The 
overgrowth of connective tissue is 
known as sclerosis, though it is more 
properly a hardening. 



SPINAL CORD. 247 

In advanced cases the posterior 
vesicular columns and nerve cells in 
the posterior cornua also degenerate 
according to the severity of the case. 
The pia mater is generally thickened 
and the posterior nerve roots and 
ganglia are nearly always degenerated 
to some extent. 

The nuclei of Goll and Burdach may 
also be affected. 

Extensive morbid changes may be 
present in the peripheral sensory 
nerves and in the optic nerves. Other 
cranial nerves may also suffer. 

Spastic Spinal Paralysis, Primary Lat- 
eral Sclerosis. The cause is obscure. 
Syphilis, infectious diseases, lead pois- 
oning and exposure to cold have been 
considered as etiological factors. 
There is a chronic degeneration of 
the anterior and lateral pyramidal 
tracts. In the lumbar region the de- 
generation is limited almost entirely 
to the lateral tracts; higher up the 
cord the anterior tracts are involved. 
The morbid changes are the same as 
in the other degenerations of the cord. 

Amytrophic Lateral Sclerosis is a com- 
bination of pathologic conditions found 
in primary lateral sclerosis and 
chronic anterior poliomyelitis. 

Ataxia Paraplegia is a combination of 
the pathologic conditions found in 
lateral sclerosis and locomotor ataxia. 

Friedreich's Disease, or Hereditary 
Ataxia, is a combination degenera- 
tion of the lateral and posterior col- 
umns. 

Syringomyelia and Hydromyelia. 

At one time these two conditions were 
considered different, but now they are 
considered practically the same. The 
condition is due to a non-perfect clos- 
ure of the central canal of the spinal 
cord during its development. The 
cord may contain one or more cavi- 
ties, or it may extend through its 
entire length. The cavities encroach 
upon the posterior coruna. 
The condition may also be caused by 
hemorrhage from injury or the break- 
ing down of gliomatous tissue. The 
cavities are surrounded by a layer of 
embryonal neuroglia tissue. 
The white matter of the cord is de- 



248 PATHOLOGY. 

ficient. The condition is met with in 
the upper portion of the cord, and as 
the cavities increase in size the wall 
will give way and the fluid contents 
will then extend to other tissues of 
the cord. The fluids are the products 
of necrosis, cerebro-spinal fluid and 
the remains of hemorrhages. 
The white tissue is dark, with sec- 
ondary degeneration of the tracts. 
Some posterior roots may be de- 
stroyed. 
4. Tumors. Glioma, sarcoma, carcinoma 
(secondary). Cysts are rare. 

THE MEMBRANES OF THE CORD. 

Dura Mater. The pathological processes 
are generally secondary to some dis- 
ease of the vertebral column. The most 
important is tuberculosis, which gives 
rise to, — 

External tuberculous pachymeningitis, 
a collection of cheesy material, un- 
dergoing softening or necrosis or con- 
tains pus cells. The dura is thickened 
and does not differ from tuberculosis 
in other serous membranes. 
Syphilis occurs as discreet gumraata 
or as regular and diffuse thickenings 
of the inner membrane. 
Tumors. Sarcoma, myxoma, lipoma, 
fibroma. 

Pia and Arachnoid. 

1. Circulatory Disturbances. Active and 
passive hyperemia from the usual 
causes. 

2. Degenerations, as calcareous and pig- 
mentary infiltrations. 

3. Inflammation. 

a. Acute Leptomeningitis, or Acute In- 
flammation, is often secondary to 
cerebral meningitis. It may be in- 
dependent, as a result of a local 
suppurative process, and may be 
serous and purulent in character. In 
the purulent an exudation is found 
on the inner surface of the dura and 
in the subarachnoidian space. If 
death does not occur adhesions may 
form between the dura and arach- 
noid. 

b. Chronic Leptomeningitis is usually 
associated with sclerosis of the cord. 
It may also follow some other in- 



NERVES. 249 

flammatory process, with formation 

of adhesions between the dura and 
arachnoid. 

Continuous pressure upon the dura 
from injury to the spinal column, etc., 

may result in thickening of the mem- 
brane. 

4. Infectious Diseases. 

Tuberculosis, as miliary nodules or 
small cheesy masses. Solitary 

tubercles may occur in any part of 
the spinal cord. 

Syphilis, appears as thickening of the 
membrane with multiple gummata 
projecting into the substance of the 
cord or involving the dura mater. 

DISEASES OF THE PERIPHERAL 
NERVOUS SYSTEM. 

THE GANGLIA OF THE CRANIAL AND 
SPINAL NERVES. t 

Ganglia of the Cranial Nerves, may be 
diseased from extension of pathologic 
processes. They are also subject to 
inflammatory changes. There is de- 
generation of the myelin sheaths and 
the nerve fibers in the ganglia. The 
cells of the ganglia occasionally un- 
dergo atrophy. The vessels are 
sclerotic. The changes are probably 
secondary to lesions in the peripheral 
sensory nerves. 

Spinal ganglia. Slight degeneration has 
been noted as a result of locomotor 
ataxia and peripheral neuritis. The 
ganglia, however, are more frequently 
involved by disease of the surrounding 
bones as cares, producing tubercular 
softening, or sarcoma, by pressure pro- 
ducing atrophy of the ganglia. 

THE NERVES. 

1. Circulatory Disturbances. 

Hyperemia, — from acute inflammation. 
Hemorrhage, — from congestion or in- 
juries. 

Edema, — from nerves traversing inflam- 
matory areas. 

2- Atrophy, in consequence of pressure 
or from disease of the nerves (neuritis) 



250 PATHOLOGY. 

or the central nervous system. Atrophy 
is sometimes seen in old age. 

3. Inflammation or Neuritis, may be di- 
vided into, — 

a. Local Neuritis, is due to cold, pres- 
sure on nerve from any cause or 
extension of inflammation from an 
adjoining tissue. 

The nerve is swollen and red. The 
sheath or the nerve fiber may be af- 
fected. 

The sheath undergoes fatty degen- 
eration. 

The fiber may become atrophied. 
If the fibers are affected the myelin 
breaks up and the axis cylinder be- 
comes irregular, granularly degen- 
erated and fragmented. 
If certain nerves are affected, spec- 
ial names are given, as sciatica, 
Bell's paralysis, brachial neuritis, 
etc. 

b. Multiple Neuritis (a number of nerve 
trunks are affected at the same time), 
may be due to sudden cold after ex- 
ertion, specific fevers, poisons as lead, 
arsenic and alcohol, diabetes, cancer, 
beri beri, etc. 

The pathologic changes are similar to 
the localized form. 

4. Infectious Diseases. 

Tuberculosis of the trunks is due to 
direct extension. It affects the roots 
and occurs in the course of tubercular 
spinal or cerebral pachymeningitis. The 
connective tissue is first affected, the 
nerve fibers degenerate slowly. 
Syphilis. The nerve roots are chiefly 
involved. There is connective tissue 
outgrowth with pressure which causes 
degeneration of the nerve fibers. Gum- 
mata is sometimes seen upon the cran- 
ial nerves. 

Leprosy. Large epithelioid cells con- 
taining vacuoles filled with the lepra 
bacillus are found within the connec- 
tive tissue of the nerve fibers. 
The small cutaneous nerves are affected 
and anesthesia and trophic changes in 
the skin are produced. 

5. Tumors. Neuroma, sarcoma, muscle 
fibers are sometimes found within the 
sheath. 



INDEX. 



Actinomycosis, 100. 

Adenoma, 72. 
Amoeba, 113. 
Aneurysm, 148. 
Anemia, 129. 
Anhydremia, 128. 
Apoplexy, 236. 
Appendicitis, 1&3. 
Arteries, 145. 
Atrophy, 29. 



Bacillus, 95. 

Coli, 97. 

Diphtheria, 95. 

Influenza, 102. 

Lepra, 106. 

Mallei, 98. 

Malignant 
edema, 99. 

Bubonic 
plague, 102. 

Tetanus, 101. 

Tuberculosis, 
103. 

Typhoid, 96. 
Bacteria, 85. 
Beri Beri, 113. 
Blastomata, 61. 
Bladder, 214. 
Blood Cells, 125. 
Blood diseases, 125. 
Bone diseases, 67- 

228. 
Bone marrow, 137. 
Brain diseases, 235. 



Carcinoma, 74. 
Chancroid, 74. 



Chancre, 108. 
Cholera, 195. 
Chondroma, 66. 



Degenerations, 31. 

Albuminous, 35 

Calcareous, 40. 

Fatty, 32. 

Glycogenic, 40. 

Hydropic, 32. 
Dipeococci, 94 
Dropsy, 27. 
Dysentry, 194. 



Edema, 27. 
Embolism, 24. 
Endothelioma, 81., 
Endocardium, 140. 
Enteritis, 191. 
Esophagus, 183. 
Epithelioma, 75. 
Etiology of dis- 
ease, 7. 



Fallopian tubes, 

222. 
Ferments, 86. 
Fever, 16. 
Fibromata, 64. 



Gall bladder, 201. 

Gangrene, 47. 
Glioma, 69. 
Glands, 

Thyroid,. 216. 

Suprarenal, 218. 

Salivary, 178. 



riaemangioma, 70. 

Heart, 16-138. 
Hemorrhage, 20. 
Hodgkin's disease, 

133. 
Hydraemia, 127. 
Hylomata, 63. 
Hydraemia, 17. 
Hypertrophy, 57. 



Inflammation, 
161. 
Lymphatic chan- 
nels, 151. 
Lymphatic glands. 

136. 
Lymphangioma, 71. 
Lymphadenoma, 71 



Immunity, 88. 
Infiltrations, 31. 
Inflammation, 49. 

Diphtheritic, 52. 

Fibroid, 52. 

Suppurative, 52 
Intoxications, 10. 
Intestines, 188. 
Ischaemia, 20. 



Jaundice, 203. 
Joint diseases, 233. 



Kidneys, 209. 

Atrophy, 210. 
Brights of, 210. 
Hypertrophy, 
209. 



Larynx, 153. 
Leucocytes, 28. 
Lepidomata, 62. 
Leukemia, 131. 
Lipomata, 65. 
Liver, 197. 

Atrophy, 197. 
Cirrhosis, 199. 
Degeneration, 

198. 
Hyperemia, 197. 
hypertrophy, 

200. 
Inflammation, 

198. 
Tuberculosis, 
201. 
Lung, 156. 

Congestion, 156. 
Edema, 157. 
Embolism, 158. 
Emphysema, 

159. 
Gangrene, 167. 
Hemorrhage, 
158. 



Malformations, 4. 

Malta fever, 112. 
Malaria, 114. 
Mammary gland. 

225. 
Metabolism, 12. 
Measles, 111. 
Meningitis, 240. 
Mouth disease, 175. 
Molluscum 

contagio<3um, 116. 
Myoma, 68. 
Myocardium, 142. 
Myxomata, 65. 
Myelitis, 244. 



Nasal cavities, 152. 
Xecrosis, 45. 
Neuroma, 69. 
Nerve diseases, 249. 
Neuritis, 250. 



Oesophagus, 183. 
Osteoma, 67. 
Osteophytes, 67. 
Ovaries, 221. 
Oidium albicans, 
103. 



Pancreas, 204. 
Parasites, 14. 
Papilloma, 73* 
Penis, 219. 
Pericardium, 144. 
Peritoneum, 206. 
Phagocytic cells, 90. 
Pharynx, 180. 
Pleura, 173. 
Plethora, 127. 
Pneumonia, 161. 

Broncho, 163. 

Fibrous, 165. 

Hypostatic, 164. 
Poisons, 10. 
Proteins, 85. 



Prostate gland, 
220. 



Rabies, 112. 
Regeneration, 55. 
Resolution, 55. 
Rheumatism, 112. 
Rhizopoda, 113. 
Rickets, 228. 



Sarcoma, 77. 
Salivary glands, 178. 
Scarletina, 110. 
Scrotum, 219. 
Seminal vesicles. 

221. 
Spirochaeta, 102- 

107. 
Spinal cord, 243. 
Spleen, 134. 
Spirillum, 98. 
Stomatitis, 175. 
Stomach, ±84. 
Staphylococci, 92. 
Streptococci, 93. 
Susceptibility, 88. 
Suppuration, 92. 
Syphilis, 108-172. 



Teeth, 179. 
Teratomata, 84. 
Testicles, 219. 
Thrombosis, 23. 
Thrush, 177. 
Thymus gland, 137. 



Tonsils, 181. 
Tongue. 178. 
Trachea, 154. 
Typhoid fever, 96. 
Typhus fever, 112. 
Tumors, ^58. 

benign, 61. 

malignant, 61. 



Urinary diseases, 

209. 
Urethra, 215. 
Uterus, 223. 



Vagina, 224. 
Vaccinia, 117. 
Varicella, 117. 
Variola, 117. 
Veins, 150. 
Vermes, 117-125. 
Volvulus, 190. 
Vulva, 224. 



Whooping cough, 
111. 

Worms, 117-125. 
Wound repair, 54. 



Xanthoma, 66. 
Yellow fever, 111, 



LIST OF ABSTRACTS 



1 . ANATOMY AND DISSECTOR IN ABSTRACT 
(Fourth Edition) (81 Illustrations), 

By Stewart L. McCurdy, A.M., M.D. 

2. PHYSIOLOGY (Second Edition) 
By Frederick A. Rhodes, M.D. 

CHEMISTRY (Third Edition), 
By John Inglis, A.B., M.D. 

4. MATERIA MEDICA AND THERAPEUTICS, 

(Third Edition). By Chas. A. Orr, A.M., M.D, 

5. HISTOLOGY 

By A. B. Wallgren, B.S., M.D. 

6. EMERGENCIES 

By Stewart L. McCurdy, A.M., M.D. 

7. PHYSICAL DIAGNOSIS AND LABORATORY 
DIAGNOSIS (Second Edition), 

By H. P. Kohberger, Ph.B., M.D. 

8. OBSTETRICS (Second Edition) 

By Wm. D. Inglis, A.M., M.D. 

9. MEDICINE (Second Edition) 

By H. P. Kohberger, Ph.B., M.D. 

10. GENITO-URINARY & VENEREAL DISEASES 
(Second Edition). (Illustrated), 

By T. L. Disque, M.D., and Geo. L. Holliday, M.D. 

1 1 . DERMATOLOGY 

By Wilton H. Robinson, M.D. 

12. VISCERAL SURGERY 

By Acheson Stewart, M.D. 

13. ARTHROSTEOPEDIC SURGERY 

By Stewart L. McCurdy, A.M., M.D. 

14. PATHOLOGY 

By A. B. Wallgren, B.S., M.D. 

15. BACTERIOLOGY 

By A. B. Wallgren, B.S., M.D. 

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